Consequently, we further hypothesize that in cases of X‐linked SCID, where even initial IL‐15 and IL‐2 STAT5 phosphorylation is compromised, in‐vivo trans‐presentation of IL‐15 (and IL‐2), via the high affinity IL‐15Rα and IL‐2Rα receptor subunits, will not be able to sustain normal peripheral NK cell numbers. The gene discussed is IL15; the disease is severe combined immunodeficiency.