The upregulation of major histocompatibility complex (MHC) and antigen-processing factors by the transcription factor Signal transducer and activator of transcription 1 (STAT1) downstream of IFNγ augments tumour antigenicity and thereby increases tumour cell recognition by T effector cells; in contrast, the duration and strength of anti-tumour responses are impeded by IFNγ-induced immunomodulatory molecules, including PD-L1, which confer immune homoeostasis11. Here, HLA-C is linked to neoplasm.