PRKN and Onset: Mutations in the PRKN gene, including point mutations and exon rearrangements, are the most common and account for up to 50% and 15% of familial autosomal recessive and sporadic early onset PD, respectively. PRKN phenotype is indistinguishable from idiopathic PD with good response to levodopa and a benign course [9]. PINK1 gene mutations are the second most frequent in familial early onset PD, compatible with recessive inheritance, and explain 1–9% of cases depending on ethnic origin.