BRAF and neoplasm: These findings were recently corroborated and expanded by 2 groups, reporting that ATP competitive RAF inhibition, through transactivation of the non-inhibited member of CRAF-CRAF homodimers or CRAF-BRAF heterodimers, leads to increased signaling through the RAF-MEK-ERK pathway in BRAF wild-type tumors, resulting in increased tumor growth [33], [34].