Interestingly, the REV1 inhibitor JH-RE-06 was recently shown to directly increase γH2AX in a colorectal cancer cell model [65], even though REV1 inhibition through JH-RE-06 does not directly elevate γH2AX in vivo during chemotherapy-induced damage [40], indicating the involvement of other cellular response mechanisms in chemotherapy damage versus post-replicative gap filling of undamaged DNA by REV1. Here, REV1 is linked to colorectal cancer.