TCHP is a tumor suppressor that regulates cell growth, apoptosis, and organellar function across multiple cellular contexts. It inhibits cell growth in bladder and prostate cancer cells by suppressing HSPB1 phosphorylation, and acts as a structural regulator of keratin filaments in epithelial cells. TCHP functions as a negative regulator of ciliogenesis, with recent evidence showing that TCHP-Aurora A signaling mediates cilia disassembly during human decidualization and is essential for endometrial stromal cell differentiation 1. Beyond ciliogenesis, TCHP localizes to centriolar satellites where it binds and stabilizes PCM1, a protein required for autophagosome maturation and endothelial cell function 2. Impaired TCHP-mediated autophagy correlates with reduced TCHP and elevated p62 levels in endothelial cells from coronary artery disease patients, and TCHP knockout mice show reduced cardiac vascularization and p62 accumulation in cardiac tissue. At the population level, TCHP variants are associated with cardiovascular disease, familial hypercholesterolemia, and autoimmune conditions; specifically, an Asian-specific splice site variant in TCHP exon 4 modulates Graves' disease risk in East Asian populations 3. These findings position TCHP as a multifunctional regulator linking autophagy, ciliogenesis, and vascular homeostasis.