CDKN2A and gastric carcinoma: Loss of p16 activity by point mutations and homozygous deletions is common in most types of cancer, however, further studies suggest de novo methylation of the 3’ end promoter region of specific CpG sites surrounding the ATG initiation codon of p16 and hypermethylation of exon 1α coding region as predominant mechanisms of p16 inactivation during tumourigenesis of gastric carcinoma [51].