Dual pathway suppression with the RET inhibitor BLU-667 and an EGFR TKI demonstrated antitumor activity both in cell lines and clinically in patients with EGFR-mutant NSCLC who had RET fusions after disease progression while receiving TKIs.23 Importantly, fusions were often seen co-occurring with multiple other known acquired mechanisms of resistance to anti-EGFR therapy in this series, which points to a diverse, heterogeneous landscape of potential resistance mechanisms adapted by RAS wild-type CRC tumors to overcome EGFR blockade. The gene discussed is RET; the disease is non-small cell lung carcinoma.