The novel SARS-CoV-2 virus is known to cause infection by gaining entry into cells with ACE2 receptors present on the surface of host cells. Recent clinical data also suggests that SARS-CoV-2 infection may potentially be augmented by Diabetes mellitus as a comorbidity factor. As the SARS-CoV-2 virus is observed to achieve entry into cells via the ACE2 receptor to engender immune response by host, the inquiry regarding upregulated cytokine storm or potential upregulation of ACE2 receptors via Diabetes mellitus Type 2 expression became apparent. A meta-analysis linking the molecular interactions from Non-Insulin Dependent Diabetes to those of Infection by SARS Coronavirus had been implemented using the Ingenuity Pathway Analysis (IPA) software under QIAGEN. Using IPA’s My Pathway tool, it was discovered that Diabetes Type 2 is associated with 948 molecules, and Infection by SARS Coronavirus is associated with 679 molecules. An overlap between the two diseases reveals that there are 79 molecules shared between the two diseases. These 79 molecules were filtered using IPA, license provided by Seton Hall University, to isolate pancreas-associated molecules, beta islet cell molecules, and cytokines individually. By filtering, it was discovered that 38 molecules are related to the pancreas, of which 5 of the 38 are associated with ACE2, named AGT, TNF, PTGS1, IL6, and AGTR1. Additionally, 13 of the 79 were discovered to be involved in beta islet cells; IL1RN, RBP4, CACNA1D, ADRA2A, NR3C1, EGR1, PPARG, GPD2, CPLX2, FOS, TP53, TNF, VEGFA. Lastly, 8 of the 79 molecules are identified as cytokines; IL1B, TNF, IL2, CCL2, IL6, IL1RN, CXCL8, and TNFSF11. Upon activation of the 5 diabetes molecules that are also associated with the pancreas and ACE2 receptors, all 8 cytokines are upregulated, not only resulting in upregulated cytokine storm in the form of Hypercytokinemia, but also upregulation of ACE2 receptors to suggest an overall increased infection by SARS Coronavirus. Additionally, activation of the 5 molecules also leads to a subsequent inhibition of 2 genes within beta islet cells, PPARG and CPLX2, as well. Thus, PPARG and CPLX2 were further explored within a new My Pathway in IPA to observe the effects on Type 2 Diabetes, insulin/glucose levels, and Hypercytokinemia via the 8 cytokines. In this pathway, it had been discovered that inhibition of PPARG and CPLX2 leads to subsequent inhibition of Insulin presence and increased glucose levels, resulting in the activation of both Diabetes Type 2, and Hypercytokinemia via activation of all 8 cytokines. Together, it has been discovered that increased expression of Diabetes Type 2 via its molecules results in immunological changes via increased cytokine storm by Hypercytokinemia alongside upregulated ACE2 expression to increase Infection by SARS Coronavirus, and increased glucose presence due to decreased insulin presence which also upregulates Diabetes Type 2 further.