The mechanism of action of HIF‐1 includes a switch from oxidative phosphorylation to glycolysis, increasing glycogen synthesis and a switch from glucose to glutamine as the major substrate for fatty acid synthesis.49 It is worth noting that the phosphorylation of AKT results in the upregulation of HIF1 in cancer cells.50 Consistent with these results, we found that PD and 2‐DG co‐treatment increased HIF‐1α by inhibit the PI3K/AKT pathway in breast cancer cell lines (Figure 5). The gene discussed is HIF1A; the disease is breast cancer.