A single study also reports ALA-dependent improvements in post-ischemic outcomes and protein kinase B (p-AKT) in a model of acute T2D [53]; however, caveolae or caveolar proteins were not assessed, and opposing effects of acute vs. chronic diabetes on ischemic tolerance [53] render acute models of limited relevance to chronic disease [42]. The gene discussed is AKT1; the disease is type 2 diabetes mellitus.