For the critical link of aberrant microglial activation in AD, highly selective small-molecule PKM2 inhibitors can be developed to disrupt the “glycolysis/H4K12la/PKM2” positive feedback loop, while designing HDAC1/3-specific cyclic peptide inhibitors to block the neuroinflammatory cascade mediated by the H3K18la/NFκB pathway [31,68,69]. This evidence concerns the gene NFKB1 and Alzheimer disease.