KRAS and colorectal carcinoma: In this regard, the timely transition of biological findings into clinical advancements (and the other way around) has allowed to consolidate several key points in the treatment strategy of CRC such as: the intrinsic dependency of CRC on the EGFR axis, the role of RAS and BRAF mutations in mediating primary and acquired resistance to anti‐EGFR agents, the need for co‐inhibition of EGFR to fully suppress KRAS or BRAF oncogenic signaling, and the potential of anti‐EGFR rechallenge (Fig. 1).