SEC23A is a core component of the coat protein complex II (COPII), essential for forming transport vesicles from the endoplasmic reticulum to the Golgi complex 1. The protein functions in cargo selection and membrane deformation during ER-to-Golgi transport 2. SEC23A mediates intracellular translocation of adipose triglyceride lipase (ATGL) under metabolic stress, regulating cardiac lipid homeostasis and preventing heart failure with preserved ejection fraction 3. While SEC23A and its paralog SEC23B share equivalent biochemical functions and interchangeable protein interactions, they exhibit distinct tissue-specific expression patterns 1. SEC23B deficiency causes congenital dyserythropoietic anemia type II, whereas SEC23A deficiency results in craniolenticulosutural dysplasia (CLSD), characterized by skeletal defects, delayed fontanel closure, and neurological impairment 4. Genome-wide association studies link SEC23A variants to circulating vitamin D levels 5. Recently, SEC23A was identified as a driver of gastric cancer progression through cell cycle regulation and tumor growth promotion 6. SEC23A expression is regulated at the transcriptional level, with mTOR signaling modulating its interaction with other COPII components to control lipogenic pathways 7.