The stability of a given EML4-ALK protein variant is associated with the stability of the corresponding fusion protein, as well as inhibitor-induced protein degradation and drug sensitivity.28 Crizotinib treatment achieved a 2-year PFS rate of 76% for variants 1/2/others vs. 26% for variants 3a/b.29 On the other hand, such differences in efficacy against different EML4-ALK variants were not observed with alectinib in patients with NSCLC.16 Therefore, the impacts of the ALK variants on the efficacy of envonalkib will have to be examined. The gene discussed is ALK; the disease is non-small cell lung carcinoma.