Thus, the increased utilization of PARP1-dependent OFM upon FANCA deficiency may confer a growth advantage to cancers with high levels of oncogene-induced replication stress where rate-limiting levels of FEN1 and LIG1 may limit cell cycle progression, potentially explaining the relatively high rate of FANCA genetic alterations in pan-cancer cohorts (Fig. 1g). The gene discussed is FEN1; the disease is cancer.