Down‐regulation of survivin expression has been shown to overcome drug resistance in acute leukaemia models.37, 49 Targeting survivin with shRNA in combination with chemotherapy also resulted in the absence of detectable minimal residual disease in a xenograft model of primary leukaemia.49 Given these findings, we sought to examine whether MUC1‐C inhibition and the subsequent decrease in survivin levels render AML cells more susceptible to standard chemotherapy. The gene discussed is BIRC5; the disease is acute myeloid leukemia.