Similarly, miR-150-5p has been proposed as a possible functional mediator of renal fibrosis in patients with IgA nephropathy, which could predict the risk of progression in this context; the presence of miR-150-5p in patients with ABMR could be conditioning the regulation of fibrosis [14], as was demonstrated in an experimental study in mice in which miR-150-5p inhibition had the potential to prevent tubulointerstitial fibrosis by suppressing the SOCS1/JAK/STAT pathway, also demonstrating that increased miR-150-5p expression in renal tissue conditions greater fibrosis. This evidence concerns the gene SOAT1 and IgA glomerulonephritis.