TVP23B (trans-Golgi network vesicle protein 23 homolog B) is a conserved transmembrane protein of the trans-Golgi apparatus involved in protein trafficking and secretion. At the cellular level, TVP23B regulates Golgi protein composition and function through interaction with YIPF6, another Golgi-resident protein 1. TVP23B is essential for maintaining proper glycosylation enzyme localization within the Golgi, as demonstrated by common deficiencies in glycosylation enzymes in TVP23B-deficient colonocytes 1. Functionally, TVP23B controls intestinal barrier integrity by regulating Paneth cell homeostasis and goblet cell function, thereby maintaining antimicrobial peptide production and mucus layer formation 1. Dysregulation of TVP23B has disease relevance across multiple conditions. In intestinal immunity, TVP23B mutation increases susceptibility to both chemically induced and infectious colitis by compromising the sterile mucin layer and host-microbe balance 1. Genetically, TVP23B variants are associated with spina bifida susceptibility as identified through exome-wide association studies 2, and the gene was identified as a convergent schizophrenia risk locus through cross-tissue transcriptome-wide association 3. Clinically, macrophage-specific silencing of Tvp23b in mice with myocardial infarction significantly improved cardiac function and suppressed pathological fibrosis 4, highlighting therapeutic potential in ischemic cardiomyopathy through modulation of macrophage-fibroblast interactions.