As chronic exposure to high levels of IL-6 has been found to mechanistically induce insulin resistance by upregulating SOC-3 expression (an inhibitor of insulin signaling) and impair insulin receptor signal transduction (Rehman and Akash, 2017), these results suggest that LSE may exacerbate immunometabolic dysregulation via elevated levels of IL-6, and downstream pathophysiological effects resembling T2DM progression. This evidence concerns the gene INS and type 2 diabetes mellitus.