KRAS and neoplasm: Since mutationally activated K-Ras 4B has an anti-apoptotic action [13,14] and, unlike K-Ras 4A, can promote cell migration [10], and K-Ras 4B can drive expression of matrix metalloproteinase 2 (MMP-2) which specifically cleaves type IV collagen, and is involved in cell detachment and migration [15], the altered splicing of the K-ras oncogene in CRC in favour of K-ras 4B could contribute to neoplastic progression by enabling the survival of cells with DNA damage and facilitating tumour invasion and, ultimately, metastasis.