BRAFV600E drives tumorigenesis through constitutive downstream ERK1/2 activation (Wellbrock et al., 2004), but hyperactivation of ERK induced by oncogenic BRAFV600E is not tolerated in the intestine: high ERK activation, induced by transgenic expression of oncogenic BRAF (BRAFV600K) or by activation of two BRAF alleles in BRAFV600E/V600E mutant mice, engages tumor suppressive mechanisms, causing loss of stem cells and induction of differentiation and senescence (Riemer et al., 2015; Tong et al., 2017). This evidence concerns the gene BRAF and neoplasm.