By my honestly shallow understanding of cancer it's not that simple.
For the cancer to not get killed immediately several things have to get broken, not just the replication inhibitor. Once they get to that state is not far fetched to think that they can have or get in the future different mutations, not specifically required to get cancer in the first place.
The comments below us talk about the folate receptor mutation that not all cancers have.
Sure but aren’t the other mutations incidental, in the sense that if we repaired the replication inhibitor the cancer would be cured in all cases? Perhaps there are even different types of replication inhibitors in different cell types, which would add complexity, but fundamentally it’s all still the same class of problem.
For the cancer to not get killed immediately several things have to get broken, not just the replication inhibitor. Once they get to that state is not far fetched to think that they can have or get in the future different mutations, not specifically required to get cancer in the first place.
The comments below us talk about the folate receptor mutation that not all cancers have.