A pioneering study on the functional landscape of resistance to ALK inhibition in lung cancer proposed several possible agents (including inhibitors of EGFR, HER2/HER3, or PKC) that might be combined with ALK inhibitors to overcome or delay a range of resistance mechanisms in ALK-rearranged NSCLC cells (H3122) with marked sensitivity to ALK–TKIs [78]. The gene discussed is PRRT2; the disease is lung carcinoma.