This could be reflective of the following: the absence of stimuli from neighboring immune cells, fibroblasts or hematopoietic/mesenchymal stem cell niches in our in vitro model; the distinct targets of BC secretome after sympathetic signaling in cells other than osteoclasts; or the intrinsic decrease in in vivo primary BC cell β2-AR expression that would explain the conditioning of the bone microenvironment in earlier stages of BC. The gene discussed is ADRB2; the disease is breast cancer.