I've just come across a patent from Fluge and Mella which looks like it was updated/published in March 2021 entitled 'Method for the treatment of chronic fatigue syndrome using an inhibitory or cytotoxic agent against plasma cells'. The description of the patent is a long read: https://worldwide.espacenet.com/pub...T=D&ND=3&date=20210304&DB=EPODOC&locale=en_EP I've selected a few random key paragraphs from the patent below which may not make total sense without reading the whole patent: 'In a first aspect, the present invention relates to a method for the treatment of chronic fatigue syndrome (CFS) comprising administering to a patient in need thereof a therapeutically effective amount inhibitory or cytotoxic agent against plasma cells' 'In particular, the present inventors recognized that an immediate or a rapid relief, e.g. within a week or weeks, from start of administration of said inhibitory or cytotoxic agent against plasma cells, e.g. by carefully increasing the dose, can be observed. In contrast to medication such as Rituximab for a treatment of CFS, which is characterized by a remarkable lag time before clinical responses, as described, e.g. WO 2009/083602'. 'Patients responding to Rituximab may have autoantibody production from immature plasma cells (plasmablasts). For most ME/CFS patients with autoantibody- production from the mature plasma cells, not responding to Rituximab, a possible way to treat ME/CFS could thus be by using a regimen that targets mature plasma cells, either because of plasma cell vulnerability to a drug with a general mode of action, or to a molecular targeted therapy directed against specific epitopes on mature plasma cells'. 'Consequently, ME/CFS can be treated with drugs that induce apoptosis and reduce autoantibody production in plasma cells. Specifically, this may be achieved by a proteasome inhibitor like Bortezomib'. 'An alternative approach for plasma cell depletion is to target the mature plasma cells directly, including memory cells, with antibodies directed toward epitopes on their surface. Such epitopes are not necessarily specific for plasma cells and must be used with care. A commercially available drug directed at CD38 (Daratumumab) is used for treatment of myeloma, because the myeloma cells typically have high densities of CD38 antigen'. 'An embodiment of the present invention, a combination of at least two inhibitory or cytotoxic agent against plasma cells may be provided'. 'In a preferred embodiment, a combination of an anti CD20 antibody and representing a biological entity of a B-cell depleting agent and Methotrexate, representing a chemical entity of a B-cell depleting agent, can be used for treating chronic fatigue syndrome of myalgic encephalomyelitis. Administration of these entities may be effected simultaneously, separately or sequentially'. 'For example, in a first regimen either the antibody or Methotrexate is administered to the subject while in a second regimen the other agent is administered'. 'In an embodiment, first the proteasome inhibitor is administered for 2-3 cycles, and thereafter, preferably with a period of time of at least two weeks, like four weeks or two months, the B-cell depleting agent is administered in four courses (1 , 2, 3 or 4 courses'. 'The administration may be systemically or locally via the enteral or parenteral way. For example, topical administration may be affected, e.g. by a patch or pavement for sustained release alternatively, an inhibitory or cytotoxic agent against plasma cells may be administered by way of inhalation or by other mucosal ways'. They also have a couple of patient examples to illustrate the invention, I assume they are real cases. Patient 2: 'Patient 2 was a woman aged 46 years, who had ME/CFS of moderate-to-severe disease severity, i.e. she was housebound and in periods more or less bedridden. She had previously participated in the open-label trial assessing cyclophosphamide intravenous infusions in ME/CFS mentioned herein, and experienced a clinical response lasting for almost a year before gradual relapse. She received the first course of Bortezomib subcutaneously at 1.0 mg/m<2>days 1 , 4, 8 and 11, with a minimal skin reaction at the injection site and no other side effects. She received the second and third courses at 1.3 mg/m<2>approximately 4 weeks apart. From 7 weeks after start of Bortezomib intervention, she experienced a gradual and consistent improvement of all her ME/CS symptoms, with increasing energy, less pain, less PEM, less dizziness and improved cognitive function. Her Fitbit armband verified her description of improvement, with increasing steps per 24 hours from mean 1500-2000 before intervention to approximately 4000, up to 7000 on single days, after response. She received in total 6 courses of Bortezomib, but after the last course she noted discomfort in her lower extremities at the legs and feet, and some constipation. She had a lasting response until 6 weeks after the last Bortezomib infusion, in total 16 weeks, before gradual relapse. Therefore, she then received Rituximab infusions 4 months apart, and has now again an increasing degree of clinical response approximately 4 months after start of Rituximab infusions'.