The data obtained from experiments and simulation indicate the following: firstly, CD40 signals are mediated by two modules of cascades of kinases; secondly, inhibition of one kinase in a module inhibits all kinases in the same module but activates kinases in the other module; thirdly, such arrangements of kinase cascades impart plasticity to the direction of the receptors signaling; and finally, based on the simulation-predicted target identification and by use of an experimental model of a parasitic infection, a putative therapeutic principle is demonstrated. The gene discussed is CD40; the disease is parasitic infectious disease.