Although the consequences of CADASIL‐causing mutations are debated [35, 36], NOTCH3 mutations might be considered the primary factor in the disease process, and the similarities between CADASIL and SVD could be explained by NOTCH3 polymorphisms associated with late‐onset SVD [35, 43], where presence of a hypomorphic NOTCH3 phenotype may render a patient more vulnerable to ischaemic processes occurring as a result of other environmental damage to blood vessel walls, such as hypertension. The gene discussed is NOTCH3; the disease is Hypertension.