PRMT7 also influences the tumor immune microenvironment by regulating immune checkpoint molecules: in melanoma cells, it acts as a coactivator of IRF-1, promoting PD-L1 expression through upregulation of the promoter H4R3me2s; the binding of PD-L1 to PD-1 on T cells inhibits T cell activity, aiding tumor immune evasion, while inhibiting PRMT7 may disrupt this evasion and enhance the efficacy of immunotherapy [175]. The gene discussed is CD274; the disease is neoplasm.