In turn, data were reported both that Erk is required for Chk1 phosphorylation and G2-M arrest induced by a microtubule disrupting agent in a colon cancer cell line [67], and that despite a requirement of the MEK/Erk pathway for an intrinsic cell cycle checkpoint that operates irrespective of DNA damage in Drosophila, the mechanism may function either together or in parallel with Chk1-dependent pathways [68]. Here, CHEK1 is linked to malignant colon neoplasm.