As to PINK1, its direct role in regulating cellular, and most specifically mitochondrial Ca2+ fluxes, has been recently proposed starting with the observation that the co-expression of mutant PINK1 in a cellular model of PD-expressing mutated α-synuclein exacerbated the observed mitochondrial defects, that is, increased mitochondrial size with loss of cristae and reduced ATP levels (Marongiu et al., 2009). This evidence concerns the gene SNCA and Parkinson disease.