Among the multiple mechanisms that mediate these contrasting effects is the interplay between canonical (Smad-mediated) and non-canonical (e.g. Kirsten rat sarcoma viral- extracellular signal-regulated kinase (KRAS-ERK), c-Jun N-terminal kinase/ p38 mitogen-activated protein kinase (JNK/p38), phosphatidylinositol-3-kinase- protein kinase B (PI3K-AKT), nuclear factor kappa B (NFκB)) signalling that are crucial for determining the differential effects on tumour suppression or tumour promotion. Here, KRAS is linked to neoplasm.