Based on our findings that inhibition of ERK phosphorylation enhanced TGF-β1-inducible NOS expression in vivo (Figure 4B), we hypothesized that ERK activation plays a pivotal role in TGF-β1-mediated control of malaria parasite development in the mosquito and that the dose-dependency of ERK activation blocks the anti-parasitic effects of TGF-β1 at the highest dose of this cytokine. The gene discussed is TGFB1; the disease is malaria.