To gain a better insight into the mechanism by which the two BTK-inhibitors reduce the cardiac dysfunction associated with sepsis, we investigated the effects of ibrutinib and acalabrutinib on (a) BTK-activation and signaling, (b) NF-κB activation, and (c) NLRP3 inflammasome assembly and activation (see below). The gene discussed is NFKB1; the disease is Sepsis.