Consequently, activated JAKs phosphorylate STAT proteins, which translocate to the nucleus to induce target gene transcription of a variety of cytokines, adhesion molecules, growth factors, extracellular matrix proteins, pro-oxidant enzymes, and scavenger receptors, leading to several pathologies related to DKD, including inflammation, oxidative stress, lipotoxicity and fibrosis [38,39]. This evidence concerns the gene SOAT1 and diabetic kidney disease.