Across diabetes, myocardial infarction, heart failure, and neuroinflammatory states, shared pathways (e.g., IL-6/STAT3, TGF-β/SMAD, PI3K/AKT, MAPK/ERK, oxidative stress) suppress neuronal excitability, promote neuron-glia-fibroblast coupling, and culminate in neurofibrotic remodeling. The gene discussed is AKT1; the disease is diabetes mellitus.