Inflammasomes are cytosolic multiprotein complexes that activate caspase-1, which promotes inflammation and host defense by driving cytokine maturation and pyroptosis. Several studies reported that caspase-1 selectively drives cytokine maturation without concomitant pyroptosis in neutrophils, yet the molecular mechanisms by which neutrophils resist caspase-1-dependent pyroptosis remain unclear. Here, we report that granulocyte-macrophage colony-stimulating factor (GM-CSF) licenses neutrophil pyroptosis upon NLRP3 and Pyrin activation by amplifying TLR4-driven inflammasome priming. Single priming with the TLR1/2 agonist, Pam3CSK4, was also sufficient to license neutrophils to pyroptosis upon NLRP3 and Pyrin activation, as Pam3CSK4 triggered superior inflammasome priming compared to LPS, the prototypic inflammasome priming agent. We further demonstrate that neutrophil pyroptosis requires autocrine TNFR1 signaling and provides genetic evidence that Ninj1K45Q/K45Q mutation disrupts plasma membrane rupture in pyroptotic neutrophils. In contrast, NLRC4 expression was not further induced by GM-CSF and therefore does not enhance susceptibility to NLRC4-dependent pyroptosis. Collectively, our data demonstrate that the inflammatory environment dictates neutrophil cell fate upon inflammasome activation.