This interpretation is consistent with previous findings in preclinical models of diabetic nephropathy by several investigators [63,64], including Qi et al. [56], showing that pharmacological activation of PKM2 was associated with recovered mitochondrial function and biogenesis, suppressed HIF-1α and lactate accumulation, blunted elevation in toxic glucose metabolites, and reduced renal inflammation and fibrosis. The gene discussed is HIF1A; the disease is diabetic kidney disease.