Liu et al. (2012) provided strong evidence in AD SAMP8 (senescence-accelerated mouse prone 8) mice models, which have age-related learning and memory deficits, that miR-16 can regulate amyloid-precursor protein (APP) in vivo and that abnormally low expression of miR-16 levels potentially lead to APP accumulation [19]. The gene discussed is APP; the disease is Alzheimer disease.