For example, endogenous H2S can ameliorate lipopolysaccharide (LPS)-induced AKI by inhibiting inflammation and oxidative stress via the TLR4/NLRP3 signaling pathway [14], and exogenous H2S (in the form of NaHS) can also provide protection from LPS-induced AKI by promoting autophagy and inhibiting apoptosis and the release of inflammatory factors [15]. The gene discussed is NLRP3; the disease is acute kidney injury.