CDKN2A and cancer: The CpG1, CpG31, and CpG32 of p16INK4a were hypermethylated and the methylation levels of these sites were negatively correlated with p16INK4a expression and cell survival rate but positively correlated with DNA damage level, suggesting that increased methylation of p16INK4a may contribute to Cr(VI)-induced cancer by lowering p16INK4a expression and causing accumulation of DNA damage [50].