Indeed, postzygotic variants in several genes involved in CVID, such as PIK3CD, STAT3, or BTK, have been detected in affected families [55], suggesting somatic or gonosomal mosaicism and thereby explaining an intrafamilial phenotypic diversity as well as occurrence of IEI symptomatology in sporadic cases without family history [56,57]. This evidence concerns the gene STAT3 and common variable immunodeficiency.