demonstrated that miR-150, which promotes renal fibrosis by downregulation of SOCS1 (antifibrotic protein suppressor of cytokine signaling 1) (104), is significantly overexpressed in urinary exosomes from patients with LN compared to healthy controls, and MIR-150 expression levels increase progressively according to the degree of LN chronicity index (CI), being most highly expressed in the high CI group (123). Here, SOCS1 is linked to lobular neoplasia.