Moreover, why there should be a distinction in CAA phenotype profiles between DS and APPdup is puzzling and it is curious why sEOAD should be more strongly associated with type 2 CAA compared to sLOAD (and vice versa for type 1 CAA), but differential possession of APOE ε4 allele does not appear to determine this. The gene discussed is APOE; the disease is Dravet syndrome.