Lin et al. reported that THSG relieved adriamycin-induced focal segmental glomerulosclerosis through activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)-Kelch-like ECH-associated protein 1 (Keap1) antioxidant pathway [41] and protected osteoblasts against H2O2-induced oxidative damage by regulating Nrf2 and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways [42]. This evidence concerns the gene NFKB1 and focal segmental glomerulosclerosis.