ANKRD13C is a molecular chaperone that regulates G protein-coupled receptor (GPCR) biogenesis and endoplasmic reticulum (ER) exit 1. The protein localizes to the cytosolic side of ER membranes and interacts with the cytoplasmic C-terminus of GPCRs, including the prostaglandin D2 DP receptor 1. ANKRD13C promotes GPCR maturation by inhibiting degradation of newly synthesized receptors, though prolonged interaction can result in ER retention and proteasomal degradation of misfolded forms 1. This chaperone activity is selective for GPCRs, as demonstrated with DP, CRTH2, TPα, and β2-adrenergic receptors 1. Pharmacologically, ligands like MK-0524 can enhance ANKRD13C-mediated DP trafficking to the cell surface, promoting DP cell surface expression by up to 50% 2. Clinically, ANKRD13C has emerged as a potential biomarker in neurological and psychiatric conditions: it was identified as a key anoikis-related gene in epilepsy pathogenesis 3 and was upregulated in PTSD patients with high intrusion symptoms, with downregulation correlating with symptom improvement following treatment 4. These findings suggest ANKRD13C as a therapeutic target for both neurological and psychiatric disorders.