These findings are particularly relevant in the context of T2DM, in which current therapeutic tools—despite the growing arsenal of agents such as metformin, sulfonylureas, GLP-1 receptor agonists and SGLT2 inhibitors—still leave a substantial proportion of patients with suboptimal control and high residual cardiometabolic risk [1,2,3,4,5,8,9,10]. This evidence concerns the gene SLC5A2 and type 2 diabetes mellitus.