Moreover, the requirement for DRH‐1 appears to be specific to viral infection, as DRH‐1 is dispensable for IPR activation in response to non‐viral triggers, such as microsporidia and proteotoxic stress.[3] DRH‐1 also activates the IPR in a manner independent of canonical RNAi components including DCR‐1/Dicer, and RNA‐binding proteins RDE‐4 and RDE‐1, suggesting that DRH‐1 upregulates transcription in a manner distinct from its effects on RNAi (Figure 3).[3]. This evidence concerns the gene PRPS1 and viral infectious disease.