β-adrenergic receptors (β-ARs) exert a significant regulatory function through the modulation of immune checkpoint molecules, resulting in the suppression of anti-tumor immune responses and the simultaneous upregulation of PD-1, TIM-3, and Lag3, ultimately leading to T cell exhaustion (Nissen et al., 2018; Acharya et al., 2020). This evidence concerns the gene CTBP1 and neoplasm.