ATF4 and Parkinson disease: Despite this, a recent work using a Parkinson-like disease mouse model has reported how sustained gene transfer–mediated ATF4 up-regulation in the dopaminergic neurons of the substantia nigra resulted in severe and caspase 3/7-dependent nigrostriatal degeneration, confirming that the PERK UPR branch plays an essential role in PD pathogenesis by activating dopaminergic neuronal loss (Gully et al., 2016).