Recent studies have demonstrated that c‐Myc activation in lung cancer cells upregulates CPT1A and further enhances the antioxidant capacity of cells through the Nrf2 pathway.[30] The c‐DTP cells exhibited a more pronounced increase in fatty acid uptake and OXPHOS compared to DTP cells, mostly likely due to activation of the c‐MYC pathway and increased CPT1A expression. The gene discussed is CPT1A; the disease is lung carcinoma.