SLFN11 and Fanconi anemia: The irreversible pathway of SLFN11 in RepStress is supported by recent findings that SLFN11 degrades stalled replication forks induced by interstrand crosslink inducers in Fanconi anemia cells, disrupts codon-specific translation process in response to DNA damaging agents, and stimulates CUL4-DDB1CDT2 E3 ubiquitin ligase to remove replication-related factors [85,132,133].