Genome-wide analysis studies in obese and CRC patients have identified hypermethylated CpG islands involved in oncogene activation, such as KRAS and solute carrier family 2 member 1 (SCL2A1), or tumor suppression, such as rho guanine nucleotide exchange factor 4 (ARHGEF4), EPH receptor 2 (EPHB2), and suppressor of cytokine signaling 3 (SOCS3), which may explain the cancer initiation in obese patients [121]. This evidence concerns the gene KRAS and colorectal carcinoma.