Using the B16 model of melanoma and the 4T1 model of mammary carcinoma, Bucsek et al showed that the reduction of β-adrenergic signalling by knocking out the β2-AR, treating mice with the β-AR antagonist propranolol or relieving chronic thermal stress with warmer housing conditions resulted in an improvement in anti-PD-1 monoclonal antibody therapy, driven by enhanced CD8+ T cell function, as evidenced by increased production of IFN-γ and granzyme B (Bucsek 2017). This evidence concerns the gene ADRB2 and breast carcinoma.