On a cellular level, HG treatment inhibited the expression of MID1, thus stimulating cellular proliferation and triggering EMT, fibrosis and inflammation of two prostatic cells via enhanced WNT/β-catenin signaling.<h4>Conclusions</h4>In general, our novel data demonstrate targeting MID1 might be a promising area of medical treatment for patients with both BPH and diabetes. This evidence concerns the gene MID1 and diabetes mellitus.