TTK and Fanconi anemia: Another, less likely, possibility would be that the helicase dead mutants are still active to an extent in vivo, despite their full loss of activity in vitro. It is noteworthy that the proposed human homolog of Mph1, FANCM, also plays a dual role: the role in checkpoint activation and replication fork progression depends on its ATPase activity [31], [39], whereas the recruitment of the Fanconi anemia core complex to chromatin (its scaffolding function) occurs independent of its ATPase domain [40].