We found that infection with lentiviral shRNA to S6K1, but not the control shRNA to GFP, downregulated the protein level of S6K1 by ~85% (vs. control), and abolished the basal or IGF-1-stimulated phosphorylation of S6K1, in Rh30 cells (Figure 4B), indicating the shRNA was working well in the cells. The gene discussed is IGF1; the disease is infection.