Previous studies have shown that the mRNA of the Btbd9 gene, the mouse homolog of the human BTBD9 gene, was down-regulated in a model of Lesch-Nyhan syndrome [6], a neurological disorder sometimes referred to as juvenile gout; and in an embryonic stem cell line that lacks the amyloid precursor proteins App and Aplp2, which are involved in synaptic formation and repair [7], [8]. The gene discussed is APP; the disease is Lesch-Nyhan syndrome.