Interestingly, the individual who developed symptoms at a later age (73 years) was heterozygous for APOE4 and had no recorded family history of cerebral microbleeds or hemorrhage, while the younger subject (54 years) was homozygous for APOE4 and the mother had an intracerebral hemorrhage that could have been consistent with CAA [23], showing that other genetic factors may contribute to the phenotypic manifestations of this mutation. This evidence concerns the gene APOE and intracerebral hemorrhage.