TNFR1 activation has been related to augmented agonist-induced Ca2+ transients, airway smooth muscle proliferation through modulation of cell mitogenesis [7], upregulation of G proteins (Gi, Gq) [17], and molecules associated with sarcoplasmic reticulum (SR) Ca2+ handling such as CD38/cyclic ADP-ribose [18]; all these effects promote airway hyperresponsiveness [19]. Here, CD38 is linked to airway hyperresponsiveness.