Several studies highlighted that miR-34a was up-regulated in patients with severe COPD and involved in the pathogenesis of COPD by affecting the HIF-1α-dependent lung structure maintenance program [22], regulating the apoptosis of human pulmonary microvascular endothelial cells by directly targeting Notch1 [23], and orchestrating the oxidative stress response by regulating the expression of SIRT1 and SIRT6 [24]. The gene discussed is HIF1A; the disease is chronic obstructive pulmonary disease.