MUC1‐C facilitates the nuclear translocation of dephosphorylated active β‐catenin that is necessary for inducing the expression of cyclin D1, MYC and survivin, a negative regulator of apoptosis.13, 14, 15 Survivin also plays a role in the proliferation and survival of leukaemia induced by the internal tandem duplication of FLT3.16 Moreover, survivin is highly expressed in AML progenitor cells and is predictive of poor clinical outcomes in patients with AML.17 Here, MYC is linked to acute myeloid leukemia.