While recent reviews have extensively summarized the role of various lysosomal genes and mutations involved in Parkinson pathogenesis identified through methods such as GWAS and family studies (including SCARB2, LRRK2, SMPD1, PARK2, PINK1, PARK7, and others), apart from SCARB2, the potential interactions between these genes and GBA1 on overall lysosomal function remain relatively uncharacterized [81–83]. The gene discussed is PRKN; the disease is Parkinson disease.