We found heterogeneity in mitotic death response within a cancer type can be attributed to mainly variation in Mcl-1 and Bcl-xL expression levels in individual cells, but not Bak, with a 2 to 3-fold difference in expression being sufficient to generate significant variation in drug-induced cell fate, i.e., dead vs. live, in a clonal population with identical genetic background. Here, BAK1 is linked to cancer.