Higher activation of CDKs, including CDK1 and CDK4, was observed in EPCAM− tumour cells compared with in EPCAM+ and Rhoj-KO EPCAM− cells after chemotherapy (Extended Data Fig. 7c–f) suggesting that RHOJ enables EMT tumour cells to progress in the cell cycle and continue DNA synthesis after chemotherapy. The gene discussed is CDK1; the disease is neoplasm.