Bacterial infection not only activates the TLR4-RIPK3 pathway via pathogen-associated molecular patterns (PAMPs) but also disrupts local immune homeostasis, promotes macrophage polarization toward the proinflammatory M1 phenotype, elevates tumor necrosis factor-alpha (TNF-α) production, and triggers Tumor Necrosis Factor Receptor 1 (TNFR1)-dependent necroptosis signaling (Weinlich et al., 2017; Brenner, Blaser & Mak, 2015). Here, RIPK3 is linked to bacterial infectious disease.