In T1DM, NF-κB activity is increased following hyperglycemia, oxidative stress-induced JNK phosphorylation (Pan et al., 2014), and reduction in insulin-induced GSK-3β phosphorylation (Wang et al., 2009; Ge et al., 2019), thereby augmenting lipid accumulation, inflammation, and fibrosis in the heart. The gene discussed is NFKB1; the disease is Hyperglycemia.