Indeed, overexpression of HHIP in COPD-derived ASMCs led to modest but significant reductions of lactate levels (Fig. 2B), decreased cell proliferation (Fig. 2C), without significant changes of mitochondrial OCR (Fig. 2D), suggesting HHIP overexpression altered aerobic glycolysis and cell proliferation rate without affecting mitochondrial OXPHOS in AMSCs. The gene discussed is HHIP; the disease is chronic obstructive pulmonary disease.