However, as highlighted in Fig. 8, which recapitulates our data in a coherent working model, the genetic/molecular background of the cancer cell being targeted crucially determines the outcome of drug interactions: indeed, depending on KRAS status and EGFR family dependence, combined BRAF/MEK inhibition may be sufficient to prevent paradoxical MAPK activation and afford synergistic growth inhibition or additional EGFR blockade maybe required to completely shut down the pathway and cell growth/survival. This evidence concerns the gene EGFR and cancer.