Model of erythroid failure during ribosome stress in zebrafish embryos and rescue with RAP-011. Multiple defects lead to the erythroid failure in zebrafish embryos upon ribosome deficiency. (i) Ribosome stress leads to lower rates of protein synthesis. (ii) Increase in p53 activity in erythroid cells lead to cell-cycle arrest and cell-death after the delay in maturation. (iii) Lft1 blocks the erythroid-promoting activity of activin/nodal signaling. (iv) Elevated MMP9 activity converts latent TGF-β to its active form. Activated TGF-β/TGF-β superfamily members induce cell-cycle arrest in erythroid cells. (v) RAP-011 sequesters and blocks active TGF-β superfamily members and Lft1 from binding to the endogenous receptor.