For example, SRRM2 contributes the tauopathies in AD by mislocalizing to cytosolic tau aggregates in brains of individuals with AD.123 HNRNPK, a splicing factor, regulates AD-driving proteoforms.124 The ribosomal protein interactors RPS14, RPS17, RPS15A, RPL21, RPS8, RPL37A, RPL14, RPS2, RPL26, FAU, RPS13, RPS24 were significantly upregulated in AD patients.125 The NFT-associated AP2A1 and AP2A250 were identified as G9a interactors that are the central hub for AD pathogenesis-associated clathrin-dependent endocytosis and postsynaptic neurotransmitter receptor internalization. This evidence concerns the gene FAU and tauopathy.