Notably, the lack of simultaneous increase in CXCL13 in ME/CFS cases implies that a subgroup of patients with ME/CFS producing excessive levels of activin A, IL-21, or a combination thereof and abnormally low CXCL13 levels exhibit defects in the normal GC reaction/Ab response, which may contribute to the immune dysfunction observed in these patients. This evidence concerns the gene IL21 and myalgic encephalomeyelitis/chronic fatigue syndrome.