Based on previous work in animals with sepsis (without T2DM), we have hypothesized that the activation of NF-κB (pro-inflammatory) and the inhibition of Akt (pro-survival) pathways are the reasons for the cardiac dysfunction in T2DM/sepsis and, hence, studied the effect of linagliptin (repurposing of linagliptin) on NF-κB inhibition and Akt activation and their impact on cardiac performance. Here, NFKB1 is linked to Sepsis.