In the condition of sorafenib treatment, AMPK has been revealed to be activated since the agent repressed mitochondrial respiration and consequently decreased ATP levels in cardiomyocytes, HCC cells, and breast cancer cells.46, 47, 48 Specifically, activation of AMPK plays a protective role against sorafenib‐induced de‐energization in hepatocholangiocarcinoma cells, revealing that AMPK depletion potentiated sorafenib treatment efficacy31 and AMPK activation contributed to sorafenib resistance. The gene discussed is PRKAA1; the disease is breast carcinoma.