Fanconi anemia (FA) is an autosomal disorder that causes genome instability. FA 
patients suffer developmental abnormalities, early-onset bone marrow failure, 
and a predisposition to cancer. The disease is manifested by defects in DNA 
repair, hypersensitivity to DNA crosslinking agents, and a high degree of 
chromosomal aberrations. The FA pathway comprises 13 disease-causing genes 
involved in maintaining genomic stability. The fast pace of study of the novel 
DNA damage network has led to the constant discovery of new FA-like genes 
involved in the pathway that when mutated lead to similar disorders. A majority 
of the FA proteins act as signal transducers and scaffolding proteins to employ 
other pathways to repair DNA. This review discusses what is known about the FA 
proteins and other recently linked FA-like proteins. The goal is to clarify how 
the proteins work together to carry out interstrand crosslink repair and 
homologous recombination-mediated repair of damaged DNA.