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). Here, CAD is linked to infection.