The excessive accumulation of inflammatory factors and neutrophils promotes the progression of inflammation and lung injury.[50] According to literature reports, inhibiting M1 polarization and apoptosis of macrophages significantly alleviates sepsis‐related ALI.[29, 51] The natural product derivative (+)3C‐20 we discovered can not only inhibit LPS‐induced inflammatory response in macrophages but also inhibit cell death caused by NLRP3 inflammasome activation. The gene discussed is NLRP3; the disease is Sepsis.