In this context, we have first found that experimental restoration of miR-1 expression in ccRCC cells leads to suppression of Caprin1, CDK4 and CDK6, cell cycle arrest at G1/S checkpoint and disrupted proliferation of the cancer cells, whereas completely silencing miR-1 further upregulates Caprin1, CDK4 and CDK6 and promotes cell cycle progression. The gene discussed is CDK6; the disease is nonpapillary renal cell carcinoma.