Pro-inflammatory cytokines and overactivation of NFκB signaling may result in dysregulation of T cell homeostasis, B cell tolerance defects, and subsequent impaired counter-select developing autoreactive B cells thus stimulating the development of autoimmunity and the clinical manifestations of AOID through the presentation of self-antigens to T cells [37]. Here, NFKB1 is linked to Autoimmunity.