Thus far, we have reviewed the evidence implicating the loss of function of TRPC6 versus the potential “gain of function” of overactivated TRPC3 in several neurodegenerative conditions, including stroke, seizures, and AD [93,94,95], painting a fascinating picture of the distinct pathological roles displayed by these two closely related members in neurodegeneration. This evidence concerns the gene TRPC3 and Stroke.