Overall, our genome-wide RNA profile provided useful knowledge to identify factors that might underlie the growth deficit (somatostatin and neuropeptide-Y) and vasodilatation phenotypes (tachykinins and Ecel1) of A-T, and to define the mechanistic overlap of A-T with the Itpr1–triggered monogenic variants of cerebellar ataxia. The gene discussed is NPY; the disease is cerebellar ataxia.