In agreement, deeper investigations in our tumor model confirmed that β3-AR antagonism, as the treatment with the anti-PD-L1 mAb, triggered cytotoxic functions of CD8+, as shown by increased number of PD1+CD8+ cells stained for perforin or granzyme B, corroborating that PD1+ TILs found in tumor mass are functionally active. The gene discussed is CD8A; the disease is neoplasm.