Our finding that neither Faslpr × Rag−/− recipients of PD-1−/− HSC, nor recipients of Prf1−/− × PD-1−/− thymocytes were spared from disease (Figures 3 and 4A,B) suggests that both of these canonical T cell effector pathways are dispensable for LIP-driven autoimmunity in the setting of PD-1 deficiency. The gene discussed is PDCD1; the disease is Autoimmunity.