In keeping with this, Gao and colleagues showed that tumours from patients resistant to α-CTLA-4 therapy harboured genomic defects in IFNγ pathway components, including copy-number loss of IFNγ pathway genes (e.g., IFNGR1/2, IRF1, and JAK2) and amplification of IFNγ pathway inhibitors (e.g., SOCS1 and PIAS4)35, while whole-exome sequencing of patient biopsies revealed loss-of-function mutations in Janus kinase 1 (JAK1) and JAK2 in patients with primary and acquired resistance to PD-1 blockade36,37. This evidence concerns the gene JAK1 and neoplasm.