These results suggest that epigenetic modulation of the NF-κB/NLRP3 inflammatory pathway contributes to neuroinflammation induced by prenatal Poly I:C exposure via enhancement of histone acetylation of H3ace and H4ace on Rela and HDAC6-mediated NLRP3 transcriptional activation (Figure 7), which may further lead to deficits in neurotransmissions and schizophrenia-like behaviors observed in offspring (Su et al., 2022). Here, NLRP3 is linked to schizophrenia.