A similar condition is thought to occur in PD due to genetic defects in LRRK2, GBA, SNCA, PARK2, PARK6, and PARK7 genes and the resultant alteration in the expression of their corresponding proteins or enzymes, i.e., LRRK2, GCase, α-Syn, parkin, PINK1, and DJ-1, which leads to the establishment of a network of several of the innate and adaptive immune cells, i.e., MOs and memory and effector T cells (43, 46–51). This evidence concerns the gene GBA1 and Parkinson disease.