As a growth arrest and starvation-linked inhibitor, GAS5 affects the Glucocorticoid Receptor (GR) [35], as demonstrated in HeLa cells, functioning as a riborepressor by acting as a decoy for the glucocorticoid response element (GRE) through specific interaction with the GR’s DNA-binding domain, thereby inhibiting DNA-dependent steroid signaling [40], shown in adipose-derived stem cells from type 2 diabetes patients. This evidence concerns the gene GAS5 and type 2 diabetes mellitus.