Fanconi Anemia (FA) is a genetic disorder characterized by the inability of 
patient cells to repair DNA damage caused by interstrand crosslinking agents. 
There are currently 14 verified FA genes, where mutation of any single gene 
prevents repair of DNA interstrand crosslinks (ICLs). The accumulation of ICL 
damage results in genome instability and patients having a high predisposition 
to cancers. The key event of the FA pathway is dependent on an eight-protein 
core complex (CC), required for the monoubiquitination of each member of the 
FANCD2-FANCI complex. Interestingly, the majority of patient mutations reside in 
the CC. The molecular mechanisms underlying the requirement for such a large 
complex to carry out a monoubiquitination event remain a mystery. This paper 
documents the extensive efforts of researchers so far to understand the 
molecular roles of the CC proteins with regard to its main function in the FA 
pathway, the monoubiquitination of FANCD2 and FANCI.