Colorectal cancers show a high frequency of activating KRAS mutations [194], and it was found that KRAS-mutated HCT116 cell line (constitutively active KRAS) shows increased stalled replication forks, pRPA32 (S33), and γ-H2AX signaling, besides the increase in RAD51 expression compared with the isogenic wild type cell line (HKe-3); all these signals together suggest a dependency on HR repair [150]. Here, KRAS is linked to colorectal cancer.