Additional signals related to hepatic stress (e.g., GGT), lipoprotein quality/function (e.g., LDL particle size, sLRP1), and adipokine-inflammation pathways (adiponectin, leptin, resistin, apelin, IL-6) further suggest a multisystem fingerprint that may help anticipate EAT expansion and downstream HF risk in T2D. This evidence concerns the gene LEP and type 2 diabetes mellitus.