This property seems to change in diseased conditions, where aberrant TRPC3 expression or function can contribute to the pathophysiology of ataxia [5,37], cardiac arrhythmias [7,38], cardiac hypertrophy [39,40,41], cardiac and renal fibrosis [42,43], to allergic airway disease [44,45], or to inflammatory hyperalgesia [46]. This evidence concerns the gene TRPC3 and cerebellar ataxia.