Our findings, that stable SOCS1 expression in HCC cells downregulates NRF2 expression and sensitizes them to cisplatin-mediated death, indicate that the loss of functional SOCS1 in many cancers [18,19,20,21,22,23,24,25,26,27,28] would allow them to withstand higher levels of oxidative stress, promote cancer progression and even promote resistance to cancer therapies that induce ROS-mediated cell death. This evidence concerns the gene NFE2L2 and cancer.