In conclusion, MVA pathway‐mediated YAP/TAZ activation converges to modulate key oncogenic processes, which are essential for driving resistance to ALK‐TKI in ALK‐rearranged NSCLC, and statin inhibits tumor growth and cell survival of ALK‐TKI‐resistant models by targeting YAP transcriptional activity. This evidence concerns the gene ALK and neoplasm.