BRAF and neoplasm: Consistent with these data, here we show that in tumor cellular contexts that are highly dependent on EGFR family signaling, such as the HER2-amplified (Calu3) and EGFR-mutant (HCC827) NSCLC cell lines, BRAF inhibition paradoxically reactivated the MAPK pathway in an EGFR/HER2-dependent manner; interestingly, we observed a similar EGFR family feedback activation in response to either BRAF or MEK inhibition in colorectal cancer cell lines and patient-derived cancer stem cells [52] (Bazzichetto C., unpublished results).