In contrast, Cdk2-deficient jck/Nek8/Nphp9 mice showed no improvement of renal cyst growth, inflammation and fibrosis, likely due to compensatory upregulation of Cdk1. In addition, treatment with the mTOR inhibitor rapamycin reduced Cdk1 and Cdk2 activity and attenuated the cystic phenotype, suggesting that the effect of mTOR inhibition is partly mediated by CDK inhibition (Zhang et al., 2020). The gene discussed is CDK2; the disease is cystic kidney disease.