In the attempt to enlighten the genetic contribution to idiopathic PD conditions, we focused on the effect of specific mutations affecting DJ-1, by measuring their outcome on: (a) DJ-1-accessory protein interactions, (b) mitochondrial morphology, (c) Ca2+ signaling, and (d) quality control via targeted autophagy, in order to reveal mutation-specific effects as well as susceptibility to damaging factors such as Ca2+ accumulation or redox events. The gene discussed is PARK7; the disease is Parkinson disease.