The mechanisms by which missense mutations drive these two syndromes differ: heterozygous dominant negative FAS mutations lead to defective signalling in ALPS patients [6], while heterozygous TNFRSF1A mutations in TRAPS patients result in endoplasmic reticulum retention of mutant proteins and exacerbated inflammatory signalling [9]. The gene discussed is TNFRSF1A; the disease is autoimmune lymphoproliferative syndrome.