This phenomenon might depend on different requirements of these genes for viability (e.g. Fanconi anaemia genes being essential in RPE1 p53-/-) or the activation of different DNA repair pathways (e.g. activation of the 9-1-1 complex vs the Fanconi anaemia pathway in RPE1 p53-/-) in response to DNA lesions generated by the absence of POLE4 (Fig. 1C). The gene discussed is TP53; the disease is Fanconi anemia.