CACNB3 encodes the beta-3 auxiliary subunit of voltage-gated calcium channels, which plays a crucial role in modulating calcium channel function and cellular excitability. As a regulatory component, CACNB3 increases peak calcium current and shifts voltage dependencies of channel activation and inactivation for both L-type (CACNA1C) and N-type (CACNA1B) calcium channels 1. The protein facilitates proper channel assembly through interactions with the endoplasmic reticulum membrane protein complex (EMC), functioning as a holdase during channel biogenesis 1. CACNB3 demonstrates tissue-specific expression patterns and functional roles beyond traditional calcium channel regulation. In immune cells, it exclusively controls ATP-dependent migration of dendritic cells by regulating inositol 1,4,5-trisphosphate receptor-mediated calcium release from the endoplasmic reticulum 2. Clinically, CACNB3 dysregulation is associated with multiple pathological conditions. Altered expression has been identified in drug-resistant mesial temporal lobe epilepsy, representing a potential therapeutic target 3. The gene also contributes to circadian rhythm regulation, with genetic variations affecting lithium's therapeutic efficacy in bipolar disorder 4. Additionally, CACNB3 serves as a diagnostic biomarker in polycystic ovary syndrome 5 and shows prognostic relevance in cervical cancer 6, highlighting its broad clinical significance across neurological, psychiatric, and reproductive disorders.