Based on preclinical data demonstrating that treatment with a defined dose and schedule of selenium resulted in the activation of Nrf2 in normal tissues and its downregulation in lung tumor tissue, it is expected that modulation of the dual function of Nrf2 by selenium will result in selective tumor tissue sensitization to subsequent treatment with immune checkpoint inhibitor-based immunotherapy alone and in combination with chemotherapy. Here, NFE2L2 is linked to neoplasm.