These cerebellar findings identify molecular mechanisms that show how ATM deficits trigger not only excessive changes in neurotransmission, but may come to impact vasodilatation/telangiectasia and inflammatory oedema (via tachykinins, Ecel1), growth and fertility (via somatostatin and neuropeptide-Y), immunity and lipid metabolism (via neurotensin), as well as pain perception (via opioids). The gene discussed is SST; the disease is telangiectasis.