TP53 and neoplasm: Although iPSCs in long-term culture preferentially use HR to cope with DNA damage,50 amplifications of tumor-promoting genes tended to occur during prolonged culture.10 Genetic aberrations in iPSCs could, at least partially, result from a transient G1/S cell cycle checkpoint deficiency,55,60 or lack of p53-mediated cell cycle arrest.61 Whole-exome sequencing revealed that the TP53 mutant allelic fraction increased with passage number of human ESCs under standard culture conditions.