CACNA1H encodes CaV3.2, a T-type voltage-gated calcium channel that operates at low voltage thresholds and exhibits voltage-dependent inactivation 1. This channel serves critical pacemaking functions in neurons and cardiac cells, and plays essential roles in aldosterone biosynthesis in adrenal zona glomerulosa cells 1. In aldosterone regulation, CACNA1H mediates calcium oscillations that govern aldosterone production in response to angiotensin II and hyperkalemia 1. Beyond endocrine function, CACNA1H is required for smooth muscle cytoskeletal organization during tracheal development, where it maintains actin polymerization through RhoA activation 2. The channel also contributes to automaticity in immature cardiomyocytes 3. Disease-wise, CACNA1H mutations cause familial hyperaldosteronism type 4, leading to excessive aldosterone production and secondary hypertension 45. Somatic mutations in aldosterone-producing adenomas represent a rare cause of primary aldosteronism 1. Additionally, CACNA1H variants are associated with intellectual disability and developmental delay, with both gain- and loss-of-function mutations contributing to neurological phenotypes 6. Decreased CACNA1H expression is also linked to congenital tracheostenosis 2, highlighting its importance in respiratory tract development.