perhaps you can rephrase this question, I did not understand:
Do RNAi molecules generally tend to show a greater correlation between the effect as seen in preclinical data versus what is ultimately demonstrated in humans as compared to other therapeutic modalities due to the nature of the therapy?
Many targets do not attack the virus or disease instead of the expression. Take a DNA gyrase inhibitor or a ribosomal disruptor. Both stop processes upstream of a phenotype. I dont know if that answers your question as I dont understand your question fully.