Finally, miR-155 was overexpressed in both human and experimental DN [28, 57], and its deletion enhanced expression of nephrin, acetylated nephrin, and Wilms tumor 1 (WT-1), a marker of podocyte differentiation, through upregulation of suppressor of cytokine signaling 1 (SOCS1) that inhibits the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 1 (STAT1) pathway [57], indicating a deleterious effect of diabetes-induced glomerular miR-155 overexpression. Here, JAK2 is linked to diabetes mellitus.