Saggese et al. confirmed the positive effect of SGLT2i on LUAD tumor burden with a different SGLT2i, empagliflozin, and characterized in detail the molecular mechanism underlying glucose starvation-induced de-differentiation: glucose deprivation causes the depletion of alpha-ketoglutarate and unbalanced activity of histone methyl-transferase EZH2 due to insufficient activity of alpha-ketoglutarate-dependent histone demethylases [87], ultimately leading to tumor de-differentiation [86]. This evidence concerns the gene PRDM9 and neoplasm.