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Background: Chk1 is involved in cell cycle arrest when DNA damage has occurred, and it plays an important role in DNA damage checkpoint, embryonic development and tumor suppression (1). Chk1 is activated in response to replication blocks and genotoxic stress, via phosphorylation of serines 317 and 345 (2). Activated Chk1 can bind to, phosphorylate (at serine 216) and inactivate cdc25c (3,4 ). Phosphorylation of cdc25c prevents activation of the CDC2-cyclin B complex and prevents entry into M-phase (3, 4).