In animal studies of acute severe pancreatitis, sivelestat sodium exerted pulmonary protection by inhibiting the signal transducer and activator of transcription (STAT) or TNF-α pathway [26], and in septic mice administered sivelestat sodium inhibited sepsis-induced macrophage infiltration, overproduction of pro-inflammatory mediators, and activation of the serine/threonine kinase pathway, which attenuated the renal injury induced by sepsis, and exerted a certain degree of nephroprotective effect [27]. The gene discussed is SOAT1; the disease is pancreatitis.