NETosis is a term that evolved following publication of an original article supposedly describing a novel form of programmed neutrophil death which resulted in the formation of neutrophil extracellular traps (NETs) (Fuchs et al., 2007). NETosis was subsequently added to the cell death classifications, almost joining the ranks of other, better documented pathways such as apoptosis, necroptosis, autophagic cell death, etc., (Galluzzi et al., 2012a). Fuchs et al. (2007) article seems to NETosis converts to be so seminal that reviewers deny publication to manuscripts in this area which fail to reference it (Amini et al., 2016; see Supporting Information; Peer Review Correspondence: URL: Link 1).We have been puzzled by the ready acceptance of a proposed programmed cell death in this format. Let us examine the phenomenon of NETosis as it is cited in the recent literature and see why this concept seems inconsistent with the economy of nature. NETosis is described as a death process in which the plasma membrane ruptures, allowing chromatin release following the collapse of the nuclear membrane (Fuchs et al, 2007). This is supposed to happen in order to rescue and protect the affected environment and this theory has been promoted by many reputable scientific journals including Nature (videos: Link 2). However, thus far no explanation has been offered as to how the remains of neutrophils that have undergone NETosis would be eliminated under in vivo conditions. This lack gives pause because such residue must be expected to be harmful to the host. In fact, under physiological conditions in healthy individuals, nuclear DNA release following activation of neutrophils encountering microorganisms is still controversial and the question has been raised whether NETosis would be at all beneficial to the host (Yipp et al., 2013).We argue that under physiological conditions, NETosis would be a wasteful, destructive process. NETosis implies a waste of neutrophils, but more importantly, it would mean exacerbated inflammation. We propose that it is important for neutrophils to remain alive for their physiological life span in order to exercise their useful skills like phagocytosis of invading microorganisms and extracellular killing of pathogens by the programmed release of mitochondrial DNA (mtDNA) and granule proteins. Neutrophils may subsequently die through apoptosis (Conus et al., 2008) or, under inflammatory conditions, also by programmed necrosis (Mihalache et al., 2011). In both cases, recognition of the dying cells by phagocytes would assure disposal without unnecessary inflammation. Mature neutrophils are terminally differentiated white blood cells that depend on glycolysis for ATP production; hence, they can afford to lose mtDNA in response to invading microorganisms. In addition, mitochondria are evolutionary endosymbionts derived from bacteria which carry bacterial molecular motifs (Zhang et al., 2010) and are considered to be master regulators of danger signaling (Galluzi et al., 2012b). Unmethylated mtDNA, like bacterial DNA, is the most potent activator of plasmacytoid dendritic cells (pDCs) and the type I interferon (IFN) pathway (Wang et al., 2015; Lood et al., 2016; Caielli, et al., 2016, and our own unpublished data). In our view, the innate immune system attempts to overcome an infection primarily with a combination of mtDNA-containing NET formation and phagocytosis. Thus, in case of persisting infection, release of mtDNA has the additional advantage of boosting the adaptive immune response. However, there would be no exaggerated inflammation caused by a “suicide bomb”. In fact, the clearance of NETs occurs in an immunologically …