Th17 cells have been implicated in the pathogenesis of human immune diseases, e.g., Crohn’s disease.50 We have further noted that inhibitors of ASM block both STAT3 and mTOR signals and limit Th17 responses in the inflamed tissues of patients with active Crohn’s disease.3 The data indicate the pivotal role of ASM-dependent intracellular signaling transduction in mediating T-cell activation and promoting Th17 responses in human diseases, as illustrated in Figure 1. This evidence concerns the gene STAT3 and Crohn disease.