On the other hand, “switch-off” mutations in tumor suppressors, such as p53 (tumor protein p53), retinoblastoma (Rb), phosphatase and tensin homolog (PTEN), von Hippel–Lindau (VHL) tumor suppressor, and CDK4 inhibitor P16-INK4 (p16INK4), turn off their functions and mitigate the ability to combat malignization [24]. This evidence concerns the gene CDKN2A and neoplasm.