In addition to G2 checkpoint abrogation in p53 defective cells, increased S phase damage thus represents another reason for tumor-selective effects of Chk1, ATR, and Wee1 inhibitors (Figure 2; Sørensen and Syljuåsen, 2012; Do et al., 2013; Lecona and Fernandez-Capetillo, 2014). Here, TP53 is linked to neoplasm.