We recently reported that the expression of 45A [2], a pol III-transcribed ncRNA, perturbs the intracellular content of FE65L1 (APBB2, amyloid beta (Aβ) precursor protein-binding, family B, member 2, NP_004298.1), a protein potentially involved in the pathogenesis of Alzheimer disease (AD) due to its binding to amyloid precursor protein (APP, P05067) [3], [4]. This evidence concerns the gene APP and early-onset autosomal dominant Alzheimer disease.