SETD8 contributes to high-risk neuroblastoma growth and apoptosis resistance by silencing p53 [13]; SETD8 promotes the carcinogenesis of colorectal cancer via deregulating the expression of PCNA [14]; SETD8 also represses the ferroptosis of pancreatic cancer cells by downregulating RRAD [15]. This evidence concerns the gene KMT5A and neuroblastoma.