For example, about 40% of colorectal cancers have mutations in K-Ras accompanied by the downstream activation of mitogen-activated protein kinase (MAPK) signalling, which promotes tumour invasion and progression since tumour cells with high MAPK activity resided specifically at the leading tumour edge, ceased to proliferate, underwent epithelial-mesenchymal transition (EMT), and expressed markers related to colon CSCs (Blaj et al., 2017). This evidence concerns the gene KRAS and neoplasm.