Moreover, they found that interferon-γ (IFNγ), which is released in the tumor microenvironment primarily by various immune cells, can induce a pro-persistence signal that is dependent on the signal transducer and activator of transcription 1 (STAT1), and IFNγ/STAT1-mediated persistence can be specifically eliminated by inhibition of type I protein arginine methyltransferase (PRMT) with MS023. This evidence concerns the gene IFNG and neoplasm.