Moreover, genetic inhibition of caspase-activated DNase (Cad), an endonuclease that mediates DNA fragmentation during apoptosis, through overexpression of its endogenous inhibitor Icad [38], together with pharmacological inhibition of Caspase-9 (Ac-LEHD-CMK), a key enzyme of the intrinsic apoptotic pathway, confirmed the involvement of neutrophil apoptosis during infection, yielding the same outcome as Casp3 inhibition (Fig. S3A–D). This evidence concerns the gene CASP3 and infection.