do Carmo et al. (2017) performed an experimental combined treatment of Chagas disease using both deoxyconformycin (a potent ADA inhibitor) and 3`-deoxyadenosine (adenosine analogue). According to the authors, the results observed in the experiments, which include reduced parasitemia and cardiac inflammatory infiltrates, are due to the modulation of seric NTPDase and ADA activities (do Carmo et al., 2017). Similar results were observed when mice were infected with T. evansi (Dalla Rosa et al., 2013; Dalla Rosa et al., 2015) and T. brucei (Rottenberg et al., 2005). This evidence concerns the gene ADA and parasitic infectious disease.