Of relevance to our research focus, the positive crosstalk between tyrosine kinases/KRAS/ERK activity and the deregulated by mutations WNT/beta-catenin activity may result in levels of WNT/beta-catenin transcriptional activity that exceed the optimal for proliferation levels that are maintained by mutations (e.g., mutations in APC, CTNNB1, etc.), and such hyperinduction of WNT/beta-catenin signaling has been shown to trigger apoptosis in CRC cells [40,41]. This evidence concerns the gene KRAS and colorectal carcinoma.