The role of SOCS1 as a tumor suppressor has been well established and some of the underlying mechanisms include attenuation of mitogenic cytokine and growth factor signaling via the JAK-STAT and RTK pathways, inhibition of oncogenic signaling proteins by promoting their ubiquitination and proteasomal degradation, prevention of the oncogenic potential of tumor suppressors such as p21 and inhibition of NRF2-mediated tumor cell adaptation to elevated oxidative stress associated with neoplastic growth. Here, NFE2L2 is linked to neoplasm.