Dipeptidyl peptidase-4 (DPP4), or cluster of differentiation 26 (CD26), is a protein encoded by the DPP4 gene. DPP4 destroys the hormone incretin. Incretins are used by the body to help produce insulin when needed and/or reduce the amount of glucose produced by the liver. DPP4 expression is significantly dysregulated in a wide range of disease states, most notably diabetes mellitus. Dysregulation as a result of diabetes leads to over destruction of incretin, causing the body to lose control of insulin levels. These relations were discovered using the Ingenuity Pathway Analysis (IPA), an in-silica research software licensed by Seton Hall University. The MAP tool of IPA shows that inhibition of DPP4 enzyme decreases circulating concentrations of tumor necrosis factor alfa (TNF-α). TNF-α is a cytokine used in the immune system for signaling cells. TNF-α alerts other immune system cells when macrophages detect infections creating an inflammatory response. With this information, we can conclude that DPP4 levels are directly proportionate with levels of TNF-α. Since diabetes leads to unregulated over expression of the DPP4 gene and excess DPP4 enzyme, diabetic patients would have higher levels of TNF-α as a result of DPP4 levels. This hypothesis is supported by experiments done in mice where human DPP4 protein increased expression of mouse TNF-α. Since TNF-α is an inflammatory marker, higher levels would lead to increased and unnecessary inflammation. In a patient infected with Covid-19, high levels of TNF-α would lead to extra inflammation, specifically in the lungs. This inflammation would result in more severe Covid symptoms causing morbidity and mortality. It is also possible that excess TNF-α contributes to unnecessary apoptosis in the epithelial cells of a Covid patient leading to morbidity. Along with this, mouse models studying Middle East respiratory syndrome-coronavirus (MERS-CoV), it was found that DPP4 protein caused increased expression of interferon gamma (IFNγ) in mouse lungs while infected with MERS-CoV. IFNγ is a cytokine that is crucial for innate and adaptive immunity against select bacterial, viral, and protozoan infections. Microenvironmental studies in context of Covid-19 have shown strong correlation between increased levels of IFNγ and increased expression of angiotensin converting enzyme 2 (ACE-2). ACE-2 is a surface protein used as a receptor for Covid-19. Covid-19’s spikey surface protein latches onto ACE-2 and enters the host cell. Increased expression of ACE-2 leads to more potential entry points of Covid-19 into healthy cells, making cells easier to infect. These conclusions are supported by studies that cite the “gliptin” class of drugs, specifically sitagliptin, to be beneficial in the treatment of Covid-19. The gliptin drug class inhibits DPP4. This class includes, sitagliptin, vildagliptin, linagliptin, and saxagliptin.