In this study, we took advantage of the lung cancer cell model with clear mesenchymal‐like phenotype acquired via EMT (mesenchymal‐type lung cancer cells) [7, 10] and demonstrated that high‐AXL expression in mesenchymal‐type lung cancers, which contributes to doxorubicin resistance, was induced by high YAP/TAZ activity upon doxorubicin treatment. This evidence concerns the gene AXL and lung cancer.