The study investigated the importance of the CD79B gene, a key component of B-cell receptors, in myelodysplastic syndromes (MDS) and acute myeloid leukemia (AML). The researchers analyzed public MDS microarray databases, prioritized CD79B, and verified its expression in clinical samples from patients with MDS, MDS transformed into AML, and controls. CD79B expression was consistently decreased in MDS and AML versus normal controls in all datasets examined. In HL-60 cells, forced expression of CD79B slightly altered cell cycle distribution and increased apoptosis. Transcriptomic analyzes linked higher CD79B expression to immune response, T-cell activation pathways, and global patterns of immune cell infiltration. The findings suggest that downregulation of CD79B is a recurrent feature of MDS and AML and may influence leukemia cell behavior and the immune microenvironment.