In conclusion, TSD upregulated KLF2 expression by inhibiting HDAC4, HDAC5, and HDAC7 and alleviated endothelial inflammation through regulation of the KLF2-dependent NLRP3/Caspase-1/IL-1β signaling pathway (Figure 7). The gene discussed is NLRP3; the disease is Tay-Sachs disease.