We recently identified a recurrent mutation in the ribosomal gene RPL10 that results in substitution of residue arginine 98 by a serine (R98S) of the ribosomal protein L10 (RPL10) in the contest of T-cell acute lymphoblastic leukemia (T-ALL). To gain insights into the mechanisms by which the RPL10 R98S mutation contributes to T-ALL development, we screened for proteins that are differentially expressed between RPL10 wild type (WT) and RPL10 R98S (R98S) expressing cells. These experiments were conducted in the mouse pro-B Ba/F3 cell line, a well-established hematopoietic model for oncogenic studies.