The potential importance of the evolution of such complex host-worm epigenetic regulatory networks is highlighted by evidence that CD4 T cells, from children recently exposed to tuberculosis and infected with the related Schistosoma haematobium showed profound differential DNA methylation, relative to those from uninfected children, that was associated with TH2-skewing of tuberculosis (TB)-specific responses away from the protective TH1/IFNγ phenotype [63]. This evidence concerns the gene IFNG and tuberculosis.