N-acetyltransferase 1 (NAT1), a polymorphic Phase II enzyme, is crucial for metabolizing heterocyclic and aromatic amines. It is involved in multiple biological processes, including drug metabolism, and is associated with various diseases [1,4,5].

In colorectal cancer, Nat1 overexpression inhibits the PI3K/AKT/mTOR signaling pathway, suppressing the epithelial-mesenchymal transition (EMT) process, glycolytic ability, and VEGF expression, thus reducing liver metastasis [2]. In breast cancer, NAT1 deletion leads to upregulation of cytidine deaminase, and NAT1-knockout cells show differential sensitivity to certain drugs [3]. In children exposed to second-hand smoke, NAT1 genetic variation increases the risk of asthma [6]. In mice, Nat1 deficiency is associated with mitochondrial dysfunction and exercise intolerance [7].

In conclusion, NAT1 plays essential roles in drug metabolism and is closely related to the development of several diseases such as colorectal cancer, breast cancer, and asthma. Mouse models with Nat1 deficiency or overexpression have provided valuable insights into the mechanisms underlying these disease-related processes, helping us better understand the functions of NAT1 in health and disease.