CDKN2A and lip and oral cavity carcinoma: For example, one study identified that p16/INK4A, an inhibitor of cyclin CDK and G1/S cell cycle progression, has been frequently reported as a target for inactivation in many oral cancers; however, SCC-25 cells were found to contain a homozygous deletion of p16/INK4A, while SCC-15 cells demonstrated hypermethylated promoter deactivation of this gene, suggesting that even the mechanisms involved in oral carcinogenesis among these cell lines are not equivalent [34].