Whereas upregulation of proapoptotic proteins like Bak and Bax are demonstrable in lower-risk MDS, an increase in antiapoptotic proteins, including Bcl-2, Bcl-XL, and the Flice inhibitory protein (FLIP), was observed in high-risk MDS during progression to AML, due in part to NF-κB inhibition of apoptosis and cell proliferation (52, 53). The gene discussed is BAK1; the disease is myelodysplastic syndrome.