We infer that relatively intact SUV39H1 expression ensures the initiation of eosinophilic inflammation in patients with Th2 skewing, which was proved in a mouse model of asthma, reported suppressed SUV39H1 to skew T cell responses towards the Th1 response, whereas functioning SUV39H1 ensured Th2 lineage stability [9]. The gene discussed is SUV39H1; the disease is asthma.