Trauma is the number one cause of death for Americans between the ages of 1 and 46. With this, 30 to 40% of trauma-related deaths are due to severe blood losses (or hemorrhagic shock). Ischemia-reperfusion injury (IRI) is a common complication of hemorrhagic shock. IRI is a period of reduced blood flow to the tissues (ischemia) followed by the return of blood flow after treatment with fluids (reperfusion). IRI causes disruptions in essential mitochondrial functions and produces damaging reactive oxygen species, ultimately resulting in cell death. Previous studies have attempted to address this complication by exploring the protective and stabilizing characteristics of the GJA1-20k. GJA1-20k treatment reduced interleukin 6 (IL6) serum concentration in a pig model of hemorrhagic show. However, a current gap in research exists in our understanding of the pathway in which GJA1-20k affects IL6 metabolism to protect tissues. We hypothesized that GJA1-20k reduced IL6 production in the liver. To test our hypothesis, we used renal and hepatic tissues from pigs treated with GJA1-20k or saline (N=6/group). We quantified IL6 transcription by rtPCR and performed immunohistochemistry to quantify IL6 expression. The control group had a statistically significant higher average expression of IL6 stain intensity compared to the pigs treated with GJA1-20k. Thus, suggesting that GJA1-20k could decrease IL6 production.