F2 and diabetic kidney disease: 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.