Wu et al. revelated that the lack of phosphatase and tensin homologue deleted on chromosome ten (PTEN) could promote the ASMC proliferation and migration, and induce airway remodeling in asthma; the inhibition of the TNF-α stimulation and the cluster of differentiation 38 (CD38)-mediated Ca2+/cyclic AMP response-element binding protein (CREB) signaling mediated by PTEN may act as the potential molecular mechanism in that [36] (Figure 1). The gene discussed is CD38; the disease is asthma.