NR3C1 and type 2 diabetes mellitus: Since GR is supposed to bind pro-inflammatory transcription factors such as NF-kappaB as a monomer [45], and since GR likely induces expression of some genes involved in gluconeogenesis (Phosphoenolpyruvate carboxykinase 1 (PCK1) and Glucose 6-phosphate (G6PC), potentially leading to type 2 diabetes mellitus, an important side effect of GCs), as a dimer [14], this led to the paradigm that beneficial, anti-inflammatory, effects were monomer mediated and that undesirable side effects were dimer mediated.