At the molecular level, CC can improve arthritis by regulating Wnt1/β-catenin, PI3K/AKT/mTOR and NF-κB signaling pathways, inhibiting the expression of pro-inflammatory factors such as interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase (iNOS), etc (Zhao et al., 2014; Zhou et al., 2019; Shen et al., 2020; Chen et al., 2023). The gene discussed is NFKB1; the disease is arthritic joint disease.