Conventional adenomas progress to carcinoma mainly through successive accumulations of CIN, a pathway that mostly begins with mutations in the adenomatous polyposis coli (APC) gene, which in turn affects Kirsten rat sarcoma viral oncogene homolog (KRAS) activation and mutations in the phosphoinositide 3‐kinase catalytic subunit alpha and SMAD family member 4 genes and subsequent heterozygous deletions of chromosome 18 and loss of TP53 function [11]. This evidence concerns the gene KRAS and carcinoma.