While UCH-L1 has been shown to inhibit α2-adrenergic receptor (AR) agonist-mediated activation of ERK via a direct association with α2A-AR receptor implicating a role of UCH-L1 in neuro-protection [32], it has also been documented that UCH-L1 up-regulates oncogenic β-catenin/TCF and Akt signaling to induce tumor cell proliferation and migration contributing to tumor progression [33], [34]. The gene discussed is AR; the disease is neoplasm.