On the other hand, RAF activation has been shown to be crucial to RAS-mediated transformation and its inhibition, by either isoform-selective or non-selective inhibitors, appears to be essential for effective downstream MEK/ERK inhibition [18] and strikingly synergizes with MEK inhibition in controlling tumor growth and overcoming resistance, particularly in KRAS mutation-driven contexts [19, 20]. This evidence concerns the gene RAF1 and neoplasm.