Two recent studies reported that exogenous TGF-β enhanced rhinovirus replication in fibroblasts and BECs and that this was accompanied by reduced interferon levels.16,17 The latter study also reported that anti–TGF-β treatment of BECs from asthmatic patients was accompanied by reduced suppressor of cytokine signaling (SOCS) 1 and SOCS3 gene expression,17 possibly associating these SOCS proteins with interferon deficiency, but no investigations of SOCS function were performed. The gene discussed is TGFB1; the disease is hyperinsulinemic hypoglycemia, familial, 4.