Nonetheless, inhibition of Rac1 in pancreatic cancer cells with a specific inhibitor or a dominant negative mutant of Rac1 is sufficient to abrogate the IR-induced G2 checkpoint activation, as evidenced by cell cycle analyses, histone H3 phosphorylation, and activity assessments of ATR/Chk1 and ATM/Chk2 kinases (see Fig. 3–6). Here, ATR is linked to pancreatic neoplasm.