For instance, blockade of the JAK–STAT3 pathway in PTEN-null prostate cancers induced the TME to become more immunogenic and to be infiltrated by increased numbers of T cells.46 In this way, tumours could be primed to respond to anti-PD1 or anti-PD-L1 therapy as the immune cells in the TME can be induced to better recognise tumour cells. The gene discussed is STAT3; the disease is neoplasm.