In this model, we propose the deletion of C/EBPβ de-represses p53 and sensitizes tumor cells to the DNA damage induced by oncogenic Ras/tumor stress, and this coupled with an induced type-1 IFN response further activates the de-repressed p53 producing a positive feedback loop, which initiates extrinsic apoptosis signaling and tumor regression through the TNFR and death receptor pathways67,68. The gene discussed is TNFRSF1A; the disease is neoplasm.