In summary, the partial molecular mechanism of IH‐related cognitive impairment is that IH enhances the SUMOylation of NEMO and decreases the level of NEMO and the expression of IκB‐α, and de‐conjugated NF‐κB is transported into the nucleus of microglia to promote the NF‐κB‐dependent inflammatory gene transcription and then creates the inflammatory response. The gene discussed is NFKB1; the disease is isolated hemihyperplasia.