Further, ex vivo cellular toxicity of apoptin decapeptide among both Imatinib resistant and Imatinib susceptible CML patient derived samples (Fig. 4 e-f) and mimicking the full length apoptin in inhibiting the BCR-ABL1 downstream signaling of c-Myc (Fig 5 a-c) illustrates the potentiality of the apoptin derived peptide for further treatment of CML. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.