Akin to this analogy, gain of function (GOF) mutations affecting stimulatory signaling pathways—pushing the throttle—lead to lymphoproliferation and autoimmunity, as seen with PIK3CD (encoding the phosphatidylinositide 3-kinase p110δ subunit); while loss of function (LOF) defects that decrease or abolish inhibitory signaling pathways—releasing the brakes—result in similar consequences, as observed in CTLA-4 (cytotoxic T lymphocyte antigen-4) haploinsufficiency and LRBA (lipopolysaccharide-responsive and beige-like anchor) deficiency. This evidence concerns the gene CTLA4 and Autoimmunity.