To explore alterations of sterile inflammation as a potential contributor to human Fanconi anemia pathogenesis we also mined human FA RNA sequencing data21 and found significantly elevated levels of IFN-α receptor-1(IFNAR1), IFN-α receptor-2 (IFNAR2) and IFN-γ receptor-2 (IFNGR2) genes in human FA patient HSPCs (Fig. S5E). The gene discussed is IFNAR2; the disease is Friedreich ataxia.