Our previously published data demonstrated that the aberrant activation of NLK in early erythroid progenitors in DBA results in phosphorylation of the mTORC1 complex on S863 of Raptor (14); from the data in Figure 1 we conclude that this phosphorylation of Raptor reduces the activity of mTORC1 leading to a decrease in phosphorylation of downstream substrates 4E-BP1 and S6K by mTORC1 in human and mouse models of DBA. The gene discussed is RPTOR; the disease is Diamond-Blackfan anemia.