The stable binding of quercetin to HAS2 implies that it may disrupt the above hypothesized regulatory loop by targeting HAS2 inhibition, indirectly inhibit TGF-β → HAS2 → HA → TLR axis-mediated ECM deposition and also inhibit fibroblast proliferation by regulating the cell cycle, thereby improving keloid. This evidence concerns the gene HAS2 and keloid.