The persistent stimulation of the immune system in subjects with chronic T. cruzi infection may induce continuous activation of IL-27/IL-27R and IL-7/IL-7R, which could lead to increased constitutive phosphorylation and gene expression of different STAT molecules, particularly observed in patients with advanced cardiomyopathy, accounting for the low degree of STAT phosphorylation in response to IL-27 and IL-7 [14,35] in these subjects. The gene discussed is SOAT1; the disease is cardiomyopathy.