Moreover, we have demonstrated that rebound increase in TRPM2 expression, which is resistant to modulation by osimertinib, in EGFRm NSCLC with acquired osimertinib‐resistance and tissues relapsed from EGFR‐TKI treatment, is a critical mechanism accounting for the emergence of acquired resistance to osimertinib since genetic suppression of TRPM2 expression by gene knockdown in osimertinib‐resistant EGFRm NSCLC cells substantially sensitized the cells to generate ROS and DNA damage, undergo apoptosis and slow down growth in vivo upon osimertinib treatment. Here, EGFR is linked to non-small cell lung carcinoma.