Similar to our observations in Nostrill knockdown cells, the knockdown of selected ISGs in IEC4.1 cells resulted in a significant suppression of IFN-γ-mediated epithelial defense, as evidenced by a higher infection burden in the siR_ISGs-treated and IFN-γ primed cells compared to those treated with the siR_Ctrl (Figure 5E). This evidence concerns the gene IFNG and infection.