The Metabolic Syndrome (MetS) is a multi-faceted disease that is prevalent in an estimated 25% of the United States population. MetS presents itself as a chain of disorders encompassing obesity, dyslipidemia, hypertension, and insulin resistance, which collectively increase an individual’s risk for cardiovascular disease and diabetes. PRCP (angiotensinase C) is a protein coding gene that we have identified as having a possible causal relationship to MetS. PRCP specifically codes for lysosomal prolylcarboxypeptidase, which cleaves C-terminal amino acids linked to the renin-angiotensin system. More importantly, PRCP regulates the cleaving of _-melanocyte stimulating hormone (_-MSH), which when cleaved, prevents the ability to inhibit food intake. RNA-sequencing and fragments per kilobase of exon per million sequence reads (FPKM) have shown PRCP as being upregulated in the Lyon Hypertensive (LH) rat, the MetS sensitive rat strain, and downregulated in the Lyon Normotensive (LN) rat, the MetS resistant rat strain. Quantitative real-time PCR (qPCR) was used to validate gene expression in PRCP liver tissue in both the LH and LN rat strains, as well as the parents. Promising results have shown PRCP to be upregulated in LH and downregulated in LN strains respectively."