Investigation recently foundthat increased NGF in asthma could induce functional redundancy of rat AMCC, whichresulting in transforming them into sympathetic neurons, and significantly reducedthe synthesis and release of EPI, unbalancing bronchial contraction andrelaxation[14],[15].Exposure tohigh level of NGF in the intrauterine environment may play an important role in theprocess of neural stem cell growth, migration and development and thedifferentiation of AMCC into sympathetic neurons, interfering with the synthesis,storage, release of EPI, even participating in adult bronchial asthma. The gene discussed is NGF; the disease is asthma.