From a pathophysiological perspective, the pathogenic mechanisms of TG can be summarized as follows: first, at the biomechanical level, TG accumulation forms a positive feedback loop with obesity, accelerating cartilage matrix degradation by increasing joint load on the one hand, and on the other, promoting the abnormal secretion of pro-inflammatory cytokines such as IL-6 and TNF-α, as well as adipokines such as leptin and resistin, thereby creating an inflammatory microenvironment with both local and systemic interactions (23). The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.