HBEGF and asthma: In summary, the growing perception that S1P is an important pro-inflammatory mediator in asthma and other inflammatory diseases (35–37), its ability to induce pro-fibrotic changes in lung fibroblasts (10) and our present findings that it may facilitate, through upregulation of HBEGF expression and other mechanisms, the mechanotransduction pathway caused by bronchoconstriction which results in remodelling all pinpoint S1P as a key molecular target in asthma, particularly in view of its potential insensitivity to corticosteroid inhibition.