KRAS and neoplasm: The underlying mechanism was shown to be that APC loss leads to both nuclear accumulation of β-catenin and stabilisation of oncogenic KRAS which, then, via the ERK pathway, further enhances and fuels activated WNT/β-catenin signalling and establishment of CSC characteristics, including enhanced sphere-forming capacity, tumour size and weight, and expression of CSC markers (e.g., CD44, CD133, and CD166) [65,69].