Remarkably, BCL‐10 knockout in CLP‐induced septic mice led to a marked reduction in NF‐κB signaling, decreased NETs formation, and alleviated organ damage, further supporting that the protective effects of Emodin in sepsis are mediated by modulating the function of the BCL‐10‐MALT1 complex to regulate NF‐κB activation and NETs formation. This evidence concerns the gene BCL10 and Sepsis.