NAT9 (N-acetyltransferase 9) is an N-acetyltransferase that mediates acetylation of N-terminal residues of alpha- and beta-tubulin, thereby stabilizing microtubules 1. Beyond its canonical acetylation activity, NAT9 functions as a chaperone protein that enhances methionine sulfoxide reductase MSRB2 activity to protect STAT2 from methionine oxidation during interferon-mediated innate immune responses 2. Loss of NAT9 increases susceptibility to viral infection, highlighting its role in maintaining immune homeostasis 2. NAT9 also suppresses c-Jun-N-terminal kinase (JNK) signaling, providing neuroprotection against amyloid-beta 42-mediated neurodegeneration independent of its acetylation function 1. Clinically, NAT9 variants on chromosome 17 (PSORS2 locus) are associated with psoriasis susceptibility, with disease-associated SNPs causing loss of RUNX1 binding near the SLC9A3R1-NAT9 region 3. NAT9 polymorphisms show associations with atopic dermatitis in some populations 4. Additionally, NAT9 is implicated in reproduction, with variants associated with litter size in livestock 5. NAT9 represents an important multifunctional regulator bridging protein quality control, immune signaling, and neuroprotection.