Many cancer types downregulate MHC-I surface display as primary or acquired immunological resistance through molecular mechanisms affecting IFNy signaling, including loss-of-function mutations in the Janus kinase (JAK) signal transducers, mutations in the IFNy receptor, and alterations in APLNR and PTPN2 genes that control IFNy sensing [4–8]. Here, PTPN2 is linked to cancer.