Hi, Cort. I, too, appreciate your highlighting this study. I think it gives us an important clue. As you know, I have proposed the GD-MCB pathophysiology model for ME/CFS. While I may seem like a stuck record, I do think that the results of this study can be interpreted in the light of this model, as follows: 1. We know from past research on the immunology of ME/CFS that this disorder involves a Th2 immune shift. 2. This means that the B cells are overactive in ME/CFS, producing antibodies. 3. However, the B cells also promote inflammation, and because of the HPA axis dysfunction that is also present, the inflammation is not well controlled by cortisol. 4. When Rituximab knocked out B cells in the patients in this study, I suggest that it also lowered the inflammation. 5. Inflammation involves the production of oxidative stress by the oxidizing free radicals that are produced by cells of the immune system. 6. Lowering the inflammation therefore would also have lowered the oxidative stress. 7. Lowering the oxidative stress would have lowered the demand for glutathione, which is the basis for the antioxidant enzyme system. 8. Glutathione would therefore have risen. 9. I suggest that in some of the patients, at least, it rose enough to correct the vicious circle mechanism involving the functional deficiency of B12, the partial block in the methylation cycle, and draining of folate from the cells. 10. I suggest that this allowed the sulfur metabolism to return to normal, and when the B cells came back up some months later, it was able to remain normal, so that the patients experienced long-term recovery. 11. For the patients that relapsed, I suggest that the new B cells produced more inflammation than the glutathione could handle, so that the vicious circle was re-established. 12. For the patients that didn't receive any benefit, even short-term, I suggest that there were other factors that were holding down the glutathione, such as high body burdens of toxins. If this is true, it might mean that doing methylation treatment together with Rituximab might improve the odds for some of the patients, so that they could also experience long-term recovery. It would be very helpful if people doing Rituximab studies in ME/CFS would monitor glutathione. I think this would give the necessary data to explain the different outcomes of the patients. Best regards, Rich