This fact has been supported by the failure to find any Flt3 (CD135) molecules on the membrane of J774.G8 cells and by experimental addition of extrinsic Flt3L to J774.G8 cells that had no effect on the multiplication of the control P13-preS2S-βgal or P13-E7 viruses at any step of infection.The inhibition of multiplication of P13-E/L-FL in macrophages might be reversible since we showed the dependence of β-galactosidase production by P13-βgal-E/L-FL on the growing activity of cell cultures. The gene discussed is FLT3; the disease is infection.