The protein thus produced has been shown to interfere with the regulation of p110δ, resulting in increased p110δ signaling and triggering activated phosphoinositide 3-kinase δ syndrome (APDS) type 2, which causes primary antibody deficiency, senescent T cells, developmental abnormalities within the T lymphocyte compartment, and immune dysregulation [91–95]. The gene discussed is PIK3CD; the disease is agammaglobulinemia.