Th17 cell deficiency can, in part, elucidate the mechanism of hypogammaglobulinemia in “predominately antibody deficiencies,” “combined T and B deficiencies,” and “associated or syndromatic features (WAS, STAT3, and ATM).” This is why the predicted Th17/Treg ratio in the PIDs patients was opposite to the that in the patients with SLE (55), vasculitis (56), and exacerbated asthma (57) who had elevated levels of Th17 cells and decreased levels of Treg cells. This evidence concerns the gene STAT3 and systemic lupus erythematosus.