CTBP1 and neoplasm: It has been hypothesized that an excess of activity of β-adrenergic receptors (βARs) may conduct to tumor development through several molecular pathways (e.g., CREB, AP-1, and NF-kB) and induce cell proliferations via β-arrestin-1 signaling, giving resistance to apoptosis by inhibition of tumor suppressor gene p53, BAD (BCL2-associated death promoter), and anoikis, a type of programmed cell death that happens when cells detach from the extracellular matrix [28–31].