These observations could be explained by the defined role of some miRNAs (hsa-miR-222/221 and hsa-miR-10a), respectively, reported to drive the activation of HSCs (101), or to upregulate the expression of TGF-β, a profibrotic growth factor (102); thus corroborating accumulating studies which report predominantly on an upregulation of fibrogenic microRNAs during schistosomiasis (103, 104). Here, TGFB1 is linked to schistosomiasis.