Interestingly, genetic alterations in several genes such as glucosidase beta acid (GBA1), leucine-rich repeated kinase 2 (LRRK2), and synuclein alpha (SNCA), among others [15], have been implicated in functional neuronal alterations, such as mitochondrial oxidative phosphorylation, autophagy–lysosomal metabolism, ubiquitin–proteasome protein degradation, endoplasmic reticulum stress/unfolded protein response, and oxidative stress (OS), as major players in the molecular development of PD [16]. The gene discussed is LRRK2; the disease is Parkinson disease.