BRAF and cancer: RTKs (and EGFR family members in particular) are a likely candidate to mediate paradoxical MAPK activation in response to inhibition of a single step of the cascade; indeed, EGFR family-mediated (re)activation of either the MAPK pathway itself or other crosstalking pathways (such as the PI3K/AKT axis) has been described in several cancer models, with or without and underlying BRAF or KRAS mutation [52, 53].