While in the model of cadmium and gentamicin-induced kidney injury, overexpression of MIOX can also aggravate the phenotype of kidney injury through oxidative stress and necroptosis [26, 27], MIOX-transgenetic mice have accelerated tubulointerstitial fibrosis when they are challenged with diabetic kidney disease [28], in our datasets, a PT cluster expressing high Miox/MIOX was found across human and mouse (Supplementary Fig. 5), according to above research results, this PT cluster may be detrimental to the kidney. This evidence concerns the gene MIOX and diabetic kidney disease.