In addition, in preclinical PCa models, METTL1 knockdown increases the secretion of cytokines involved in proinflammatory activity, which polarises macrophages to the M1‐like endotype and induces the down‐regulation of anti‐inflammatory cytokines which can polarise macrophages to the M2‐like endotype, indicating that METTL1 inhibition can polarise immune cells in the tumour microenvironment (TME) toward a cytotoxic tumouricidal endotype and enhance the response to immunotherapy.61 The gene discussed is METTL1; the disease is neoplasm.