Additionally, Wu et al. demonstrated that the decreased expression of PTEN but increased CD38 expression was observed in TNF-α-induced ASMCs, whereas the overexpression of PTEN could remarkably downregulate CD38 expression, Ca2+ levels and phosphorylation of cyclic AMP response-element binding protein (CREB), and the proliferation and migration of ASMCs, suggesting that regulating PTEN/CD38/Ca2+/CREB signaling could restrict airway remodeling and inflammation in asthma [36]. This evidence concerns the gene TNF and asthma.