CACNB1 encodes the β1 auxiliary subunit of L-type voltage-gated calcium channels, functioning as a critical regulatory protein that modulates channel activity and membrane localization 123. The protein regulates L-type channels containing multiple pore-forming subunits (CACNA1A, CACNA1B, CACNA1C, CACNA1D) and is essential for their functional expression 123. CACNB1 undergoes alternative splicing producing three isoforms (β1a, β1b, β1c) 4. Beyond canonical calcium channel regulation, CACNB1 mediates non-channel functions in T cell immunity, where it regulates clonal expansion and apoptosis independently of voltage-gated calcium current activity 5. In skeletal muscle, CACNB1 variants cause early-onset congenital muscular weakness through excitation-contraction coupling disruption 6. CACNB1 also participates in synapse vesicle release regulation and cognitive function via alternative splicing mechanisms 7. Clinically, CACNB1 emerges as a therapeutic target in hepatocellular carcinoma patients with metabolic dysfunction 8 and shows potential in cardiac pacemaker cell differentiation 9. Genetic variations in CACNB1 associate with ADHD pathogenesis, and L-type calcium channel blockade with amlodipine demonstrates efficacy in reducing ADHD-related hyperactivity across multiple species 10.