If many genes found harboring heterozygous allelic variants were once believed to have dominant transmission producing a full phenotype, nowadays we know that only the most disrupting ones have a true AD inheritance (i.e. FGFR1, CHD7), and the vast majority of pre(peri)-pubertal CHH is more likely to arise with hemizygosis (ANOS1), homozygosis, compound heterozygosity, or oligogenicity [1]. Here, ANOS1 is linked to Alzheimer disease.