Biologically, both platforms indicate a tissue specific correlation of the DEGs as observed in the PCA plots where the liver, lung, and spleen are clustered into three distinct groups. Analyses of the biological functions, pathways and networks with the core spleen DEGs showed cell growth and proliferation, cell division, cell death, and heme metabolism are common functions across all tissues and treatment conditions in 9V/null spleen. The Gene Ontologies for the common DEGs suggest that the top functions, based on the number of DEGs involved and the p value, include cell growth and proliferation, cell death and survival, and inflammation. The unique genes in the imig and vela group mainly coincided with the same functional groups with some differences. The number of genes associated with the common functions is greater in the imig treated group compared 
to vela. This suggests that even though the two drugs are very similar structurally and functionally there are differences at the molecular level. Overall functional analyses suggest overlap of some significant canonical pathways, i.e., the oxidative phosphorylation, mitochondrial dysfunction and ubiquinone Diperodon biosynthesis in the saline-treated 9V/null liver and spleen samples. Interestingly, some of the mitochondrial dysfunction genes overlapped with the heme biosynthesis pathway. The heme biosynthesis pathway is a tightly orchestrated process that occurs in all cells. In most eukaryotes, the first step in heme synthesis is the mitochondrial gene, d-aminolevulinic acid synthase, which catalyzes the reaction between succinyl-CoA and glycine to form d-aminolevulinic acid, dAla. Defects in d�CAlas2, Abcb7, Glrx5 and Slc25a38 are causal to different forms of sideroblastic anemias. These Ginsenoside-Ro exhibit mitochondrial iron overload and impaired heme synthesis. The solute carrier Slc25a39 is important for maintaining mitochondrial iron homeostasis and regulating heme levels. Mitochondrial dysfunction has been reported in lysosomal diseases in part due to the involvement of the autophagy/ mitophagy system. Recent studies suggest that mitochondrial dysfunction and subsequent ATP deficiency may be responsible for the neuronal impairment in Niemann-Pick Type C and Gaucher diseases. Mitochondrial dysfunction increases with aging and has been found in Parkinson’s and other neurodegenerative diseases. Indeed, heterozygotes for GBA1 mutations occur with greater frequency in patients afflicted with Parkinson’s disease and there is a pathogenic relationship between GCase alterations, mitochondrial dysfunction, and Parkinson’s disease. These observations and the current data support the involvement of altered mitochondrial function, hematopoiesis and myelopoiesis as important molecular processes in the progression of Gaucher disease. Jak3, in the JAK/STAT pathway, is the only hematopoietic gene with increased expression in treatment with either enzyme or saline. Both STAT3, and SOCS have been recognized for their anti-inflammatory actions. The imig and vela ERT showed increased expression of both STAT3 and SOCS suggesting that a reduction of the lipid mediated increases of inflammatory immune response via this pathway. This provide a pathway for development of therapeutics for Gaucher disease, since involvement of JAK-STAT pathway and increases of the cytokines are evident. In conclusion, this study shows that NGS technologies are able to assess the transcript abundance at the whole genome level and their response to drug interventions. With continued cost reduction and improved analytical methods, NGS has begun to have a direct impact on biomedical discovery and clinical outcome.