Indeed, Rpl22 deficiency attenuates the development of B lymphocytes and αβ-lineage T lymphocytes in a p53-dependent manner while sparing other lineages, including γδ T cells.19,20 Rpl22 also regulates the emergence of embryonic HSCs by controlling the translation of Smad1 mRNA.21 Finally, RPL22 mutations and deletions have been observed in human T acute lymphoblastic leukemia (T-ALL), and Rpl22 loss promotes lymphoma development in a mouse model of T-ALL, suggesting that it functions as a tumor suppressor.22 This evidence concerns the gene SMAD1 and T-cell acute lymphoblastic leukemia.