<title>Abstract</title>  <p><bold>Background</bold>In chronic myeloid leukemia (CML), Aurora kinase A and Polo like kinase 1 (Plk1), two serine-threonine kinases involved in the maintenance of a functional G2/M checkpoint, may cooperate with the constitutive tyrosine-kinase (TK) activity of the BCR-ABL1 fusion protein increasing DNA damage, promoting the occurrence of additional genomic alterations ultimately driving resistance to TK inhibitors (TKIs) and progression from chronic phase to blast crisis (BC). The gene discussed is MARK2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.