In contrast to the more established role of GSK3α/β as a tumor suppressor pair, which inhibits Wnt signaling via β-catenin phosphorylation and subsequent degradation6, it has been shown that GSK3α plays an important role in maintaining an undifferentiated leukemic state of AML blasts and therefore selective targeting of GSK3α, which avoids concomitant inhibition of GSK3β and β-catenin stabilization, could represent a viable therapeutic strategy in AML5. The gene discussed is GSK3B; the disease is acute myeloid leukemia.