Patients were aged 18 years or older, had stage IIIb or stage IV ALK-positive NSCLC that had progressed while they were on crizotinib therapy....The five non-EML4–ALK fusions were ALK–HIP1 (n=2), ALK–KIF5B (n=1), ALK–PPFIBP1 (n=1), and ALK–DCHS1 (n=1). 45 (31%) patients had secondary ALK alterations (point mutations or amplifications) and five (3%) patients had genetic alterations that could have mediated bypass signalling (eg, KRAS and EGFR activation; table 4)...Table 4: Efficacy of ensartinib by ALK mutation type.