We tested whether inhibiting SP1-directed transcription of dynein can rescue DN in vivo and showed that MIT treatment of STZ-induced diabetic mice indeed rescued the damaged morphology and filtering function of podocytes by preventing upregulated dynein expression, accompanied by an alleviation of albuminuria and late DN pathology, such as mesangial expansion, glomerular fibrosis, and interstitial fibrosis. This evidence concerns the gene SP1 and liver dysplastic nodule.