On the basis of previously reported fundamental principles and bioinformatics findings, we inferred that ENO1 could regulate the PI3K/AKT and AMPK/mTOR pathways by activating glycolysis and increasing ATP and lactate levels, thereby influencing stemness.24,25 As shown in Supplementary Fig. 6d, ATP production was negatively correlated with the activation of the AMPK/mTOR pathway, which is consistent with previous reports in cancer cells.26,27 We subsequently validated the effects of ATP and lactate on the PI3K/AKT signaling pathway. The gene discussed is ENO1; the disease is cancer.