They found that treatment with TLR9 agonists increased the secretion of IFN-α (a Th1-promoting cytokine) and that pDCs from IFN-β-treated clinically isolated syndrome (CIS)/RR MS patients had a significantly lower C-terminal TLR9 expression as well as IFN-α, IL-6, and TNF-α secretion compared to untreated patients (Balashov et al., 2010). This evidence concerns the gene TLR9 and in situ carcinoma.