It attenuates TNF-α and IL-1 secretion by inhibiting the phosphorylation of AKT and NF-κB p65.[26] Notably, quercetin has been observed to enhance t-PA expression via p38MAPK pathway activation, contributing to thrombosis delay and circulation improvement in KOA-affected areas.[27] Additionally, quercetin’s regulatory effect on the NF-κB pathway modulates MMP-13 and TIMP-1 gene expression in chondrocytes, thereby balancing oxidative stress responses, diminishing extracellular matrix degradation, and preserving articular cartilage. The gene discussed is IL1B; the disease is deep vein thrombosis.