Their study revealed acritical role of caspase-1−/− mice in sepsis by protectingsplenic B-lymphocytes from apoptosis, which might in turn restore natural antibodyproduction by the B cells, preventing host from bacterialpredisposition.40 However, VandenBerghe et al.41 recently opposed that finding and made a strongstatement by showing optimal protective outcomes against sepsis in terms of reducingsystemic damage, cytokine levels and mortality in those mice, which had combinedknocked-down of IL-1β and IL-18 genes, instead of those lacking onlycaspase-1. This evidence concerns the gene IL18 and Sepsis.