Remarkably, as human monocytes adhere to surfaces and begin differentiation into macrophages, they may lose their surface β2-AR and hence become insensitive to the inhibitory effects of β2-AR agonists on LPS-induced TNF-α production, an observation which has been related to the lack of anti-inflammatory effect of β2-AR agonists on alveolar macrophages or in clinical asthma (Ezeamuzie et al., 2011). Here, ADRB2 is linked to asthma.