CABP4 is a calcium-binding protein essential for normal synaptic function in photoreceptors and auditory neurons. CABP4 directly associates with voltage-gated calcium channels (Cav1.4 and Cav1.3), shifting their activation to more hyperpolarized voltages and suppressing calcium-dependent inactivation 1. This modulation is critical for regulating Ca2+ influx and neurotransmitter release at photoreceptor synaptic terminals 1. CABP4 function is dynamically regulated through phosphorylation by protein kinase C and dephosphorylation by protein phosphatase 2A, fine-tuning presynaptic calcium signals in response to light 2. Clinically, CABP4 mutations cause cone-rod synaptic disorder and congenital stationary night blindness (CSNB), characterized by early-onset reduced visual acuity, photophobia, impaired color vision, and nystagmus without nyctalopia 34. Retinal manifestations include foveal thinning and outer plexiform layer abnormalities, with stable disease course over time 56. Emerging evidence suggests CABP4 variants may also contribute to autosomal dominant nocturnal frontal lobe epilepsy through altered calcium channel regulation in cortical neurons 7. These findings establish CABP4 as a critical regulator of synaptic calcium signaling with implications for both retinal and neurological disease.