Nevertheless, based on our findings that RCAN1 gene triplication alone is sufficient to substantially disrupt NGF-dependent development of sympathetic neurons, and importantly, that these defects in Dp(16)1Yey/+ mice are significantly ameliorated by normalizing RCAN1 levels, we conclude that an imbalance in RCAN1 gene dosage is a key contributing mechanism to the sympathetic phenotypes in Down syndrome mice. The gene discussed is RCAN1; the disease is Down syndrome.