ITGAM and infection: Intuitively, the induction of apoptosis in circulating “rogue” [DEspR + CD11b +] neutrophils will pre-empt DEspR + [NET + Ns], but spare DEspR(-)[NET + Ns] and DEspR(-)neutrophil roles in key defense mechanisms against pathogens, thus likely avoiding the increases in infection risk seen in total neutrophil/NET + N inhibition or depletion.