Similar to other malignant tumors, carcinogenesis of EA is characterized by several genetic and epigenetic alterations with genetic instability (e.g., loss of heterozygote and/or ploidy), abnormal expression profiles of oncogenes (e.g., c-myc, VEGF and its receptors) and alterations in the DNA-methylation pattern (e.g., hypermethylation of p16, TIMP-3, DAPK, SOCS1 and SOCS3, and hypomethylation of CDX1. This evidence concerns the gene MYC and cancer.