Consistent with these reports of loss-of-function mutations in JAK1/2 as an innate and acquired resistance mechanism, in vivo CRISPR screening using a mouse model of melanoma demonstrated that deletion of IFNγ receptors (Ifrngr1 and Ifngr2) and JAK/STAT pathway components (Jak1, Jak2, and Stat1) resulted in resistance to PD-1 blockade (Manguso et al, 2017). The gene discussed is SOAT1; the disease is melanoma.