Figure 3E shows that levels of induction of TGFbeta were not statistically different after infection of BMPR2 WT, heterozygous or homozygous knockout iPSCs, ruling out that the differences in permissiveness of these cells were due to differences in levels of TGFbeta induction. However, if TGFbeta was neutralized during infection of BMPR2 KO-iPSCs, the latent phenotype could be rescued (Fig. 3F, left and middle graphs). This was specific for BMPR2 deficiency since removal of YY1 could not be rescued by the removal of TGFbeta (Fig. 3F, right graph), suggesting that BMPR2 acts upstream of YY1. The gene discussed is BMPR2; the disease is infection.