This pathogenic cascade, modulated by multiple additional factors (e.g., kinase-enhancing LRRK2 mutations, α-synuclein expression levels, glucocerebrosidase (GBA) gene mutations, mitochondrial dysfunction, and NOX2-activating extracellular signaling) may be a scenario best addressed by a multi-target drug strategy that impacts diverse adaptive responses and multiple pathogenic mechanisms that contribute to pathogenesis of PD. The gene discussed is GBA1; the disease is Parkinson disease.