The KRAS mutation generates a series of modifications in the mechanisms of cellular repair and the regulation of growth due to its interaction with different growth factors (primarily TGF-β1 and FGF2) and signalling pathways, such as mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)–Akt, which alter the cell proliferation of the tumour cell line, and other mutations (such as in the p16, p53, DPC4, and BRCA2 genes) and alterations in differentiation that eventually transform into a neoplastic lesion. This evidence concerns the gene TP53 and neoplasm.