Any theory that accounts for the loss of SNc DA neurons in PD must include an explanation as to why DA neurons of the VTA, or indeed calbindin-positive SNc DA neurons, are relatively spared in PD or models of PD.13, 41 It is clear that they have different molecular and physiological characteristics that contribute to the differential susceptibility3, 19, 42; however, they also have strikingly different morphological characteristics. The gene discussed is CALB1; the disease is Parkinson disease.