Given that the ALKi plus PI3Kβi combination was effective on cells derived from TP53 mutated tumor regions representing both epithelial and mesenchymal phenotypes, as well as established ALK‐rearranged H3122 (TP53 mutant) and H2228 (TP53 and NFE2L2 mutant) cell lines, our findings suggest that this combination carries promise to counteract ALKi resistance associated with EMT, TP53 or NFE2L2 mutations [3, 41]. The gene discussed is ALK; the disease is neoplasm.