The unveiled molecular basis for the disease opened a new perspective of targeted therapies, such as PI3Kδ inhibitor, leniolisib, modulating polyclonal proliferation and autoimmunity in PI3Kδ syndrome (APDS), or abatacept, a CTLA-4/FcIgG1 fusion protein effectively controlling T cell activation and autoimmune disorders in CTLA-4 haploinsufficiency or LRBA deficiency [140]. This evidence concerns the gene CTLA4 and activated PI3K-delta syndrome.