The suppression of HIF-1α resulted in the amelioration of tendinopathy and the promotion of tendon repair. HIF-1 is implicated in the pathogenesis of TP through its involvement in the NF-κB and MAPK signaling pathways. This is supported by the observation that the administration of YC-1 led to a decrease in inflammatory factors, such as IL-6, and ECM mediators, such as MMP-13. Furthermore, the upregulation of tenocyte markers, including TNC and SCX, following YC-1 treatment suggests improved tendon healing. This evidence concerns the gene NFKB1 and disease of the tendon.