NAA10 (N-alpha-acetyltransferase 10) is the catalytic subunit of the NatA complex, catalyzing N-terminal acetylation of approximately 40-50% of human proteins 1. It acetylates amino termini devoid of initiator methionine and performs lysine-specific acetylation of internal protein residues 1. Beyond canonical acetyltransferase activity, NAA10 functions as a lactyl-transferase, modifying target proteins in response to cellular metabolic conditions 2. Mechanistically, NAA10 regulates diverse cellular processes including protein stability, chaperone function, and cell cycle control. It stabilizes tumor suppressors like TSC2 and represses oncogenic kinases such as MYLK, thereby limiting cancer cell migration 1. NAA10 also promotes ferroptosis in cancer cells through multiple axes, including NSUN2 lactylation and HMOX1-dependent pathways 23. Pathogenic NAA10 variants cause neurodevelopmental disorders collectively termed NAA10-related syndrome, characterized by intellectual disability, autism spectrum disorder, seizures, cardiac anomalies, and craniofacial dysmorphology 45. Conversely, NAA10 overexpression in cancers correlates with poor prognosis, enhanced epithelial-mesenchymal transition, and resistance to cell death 6. NAA10 variants are also implicated in Jeavons syndrome (epilepsy with eyelid myoclonia) 7, suggesting tissue-specific developmental requirements for proper N-terminal acetylation.