Given that type I IFN is capable to induce B cells to express CD38 [75] that prevents apoptosis of GC B cells [76], and that B cells from CDG patients expressed higher levels of CD38 [25], it is conceivable that type I IFN response contributes to the NCF1-associated autoimmunity via inhibiting apoptosis of autoreactive GC B cells. Here, CD38 is linked to congenital disorder of glycosylation.