When the expression of these proteins decreases, as in the early stage of Alzheimer's Disease (AD), these factors are not effluxed altering the microenvironment of stem cell niche and cellular homeostasis with functional alterations in neurogenesis.1 Therefore, since the expression of ABC transporters present in hNSPCs can be modulated, these proteins are the key for promoting hNSPCs self-renewal without differentiation. Here, ABCG2 is linked to Alzheimer disease.