Therefore, it may not be surprising that the levels of secreted TGFbeta observed in cultured uninfected WT-iPSCs are too low to generate high enough levels of TGFbeta signaling to lead to SMAD2 phosphorylation in these cells but that this can occur when these levels of TGFbeta are increased by latent infection. The gene discussed is SMAD2; the disease is disease arising from reactivation of latent virus.