In particular, the positive correlation of the ADRB3 gene expression with immune-suppressive checkpoints, such as CD276, a NB-associated molecule found in unresponsive NB variants, in which exerts a protective role from an NK cell-mediated lysis [56, 57], or with CTLA4, whose inhibition was shown to be non-redundant in enhancing antitumor T cell killing in NB [58], highlighted the ability of the β3-AR signaling to sustain different mechanisms favoring tumor immune escape. The gene discussed is CTLA4; the disease is neuroblastoma.