We report here for the first time that (a) activation of BTK is associated with the activation of the NLRP3 inflammasome in septic hearts, and (b) inhibition of BTK activity with ibrutinib and acalabrutinib reduces both the assembly and subsequent activation of the NLRP3 inflammasome in septic hearts (and the cardiac dysfunction caused by sepsis). This evidence concerns the gene BTK and Sepsis.