Consistent with our findings, Plod2 knockdown decreased glycolytic energy metabolism by suppressing HK2 expression in MPCs, leading to the alteration of MPC migration and chondrogenic potential in vitro.63 PLOD2 also promotes aerobic glycolysis and cell progression in colorectal cancer by upregulating HK2.45 In addition, elevated PLOD2 expression was associated with increased cytoplasmic succinate levels for cancer cell mesenchymal phenotypes and stemness,28 further supporting our finding that the HIF-1α/PLOD2 axis regulates cell metabolism to affect the fate of HO-forming MPCs. This evidence concerns the gene HIF1A and colorectal cancer.