The inhibition of HMGB-1 reduces signalling through p38MAPK, ERK1/2, and JNK, crucial pathways in cardiac hypertrophy, fibrosis, and cytokine-mediated inflammation.60 Song and colleagues (2016), found cardiac expression of HMGB-1 in a hyperglycaemic environment is mediated by the PI3Kgamma/Akt pathway, and treatment with an antioxidant prevents PI3Kgamma/Akt signalling and HMGB-1 production, suggesting a potential therapeutic target for diabetic cardiomyopathy.61 This evidence concerns the gene PIK3CG and cardiac hypertrophy.