We identify autophagy as a defense mechanism in response to FGFR/PLK1 inhibitor‐induced surge of metabolic stress, which is consistent with recent studies showing that KRAS‐driven tumor cells depend on autophagy to help reduce ROS and to provide substrates to fuel cell metabolism (Guo et al, 2011; Yang et al, 2011, 2020; Lee et al, 2019). The gene discussed is PLK1; the disease is neoplasm.