We demonstrated the expression of the β3-AR protein in tumor-infiltrating CD4+ and CD8+, and then through selective β1-, β2-, and β3-ARs silencing, we corroborated the prominent role of the β3-AR subtype, located on lymphocytes, in controlling the IFN-γ-dependent PD-L1 expression on NB tumor cells. The gene discussed is IFNG; the disease is neoplasm.