We have previously reported that inhibition of BTK by ibrutinib or acalabrutinib attenuate sepsis-induced cardiac and renal dysfunction in C57Bl/6 mice (14) and additionally we have now shown that delayed administration of ibrutinib in WT-CLP (CBA background) also attenuates sepsis-induced cardiac dysfunction, renal dysfunction, and hepatocellular injury, confirming that BTK inhibitors work in two different genetic backgrounds of mice. This evidence concerns the gene BTK and Sepsis.