CACNA1H and irritable bowel syndrome: Experimental studies have consistently demonstrated the central role of these channels, particularly the Cav3.2 isoform, in pain modulation, and inhibition of these channels has been shown to reduce visceral hypersensitivity in animal models.11,12 In humans, Cav3.2 overexpression has been observed in the colonic mucosa of patients with IBS,13 and a prior clinical study of ethosuximide in this population suggested a potential therapeutic benefit.14 However, that study’s open-label, uncontrolled design limited its interpretability.