CHEK1 and neoplasm: The relatively acute response and short half-lives of downstream effectors (e.g., minutes for p53 and hours for CHK1) provide a tunable response based on the current level of immune targeting through stress-induced mutagenesis (Bindra et al., 2007; Rosenberg, 2001; Rosenberg and Queitsch, 2014) that in our analysis directly influences tumor-associated antigen availability.