Thus, the pharmacological modulation of the NF-κB p65/NLRP3-mediated pathway and subsequent promotion of M1 to M2 polarization can reduce neurological deficits and cerebral infarct and is a promising therapeutic strategy in the acute stage of transient cerebral ischemia (Song et al., 2021; Li et al., 2022). This evidence concerns the gene NFKB1 and brain infarction.