Abrogation of the G2 checkpoint by inhibitors of Chk1, Wee1, or ATR may therefore selectively sensitize p53 defective cancer cells to DNA damaging agents, while the surrounding normal cells could be spared (Figure 1; Leijen et al., 2010; Ma et al., 2011; Hirokawa et al., 2014). The gene discussed is CHEK1; the disease is cancer.