This is consistent with the observation that over-expression of GAPDH can prevent caspase-independent cell death in response to treatment with etoposide, staurosporine, or actinomycin D [27]; that chronic myelogenous leukemia (CML) cells resistance to imatinib therapy spontaneously upregulated GAPDH expression and that these resistant cells could be sensitized by siRNA knockdown of GAPDH expression [48]. This evidence concerns the gene GAPDH and chronic myelogenous leukemia, BCR-ABL1 positive.