Fanconi anemia (FA) is a complex cancer susceptibility disorder associated with 
DNA repair defects and infertility, yet the precise function of the FA proteins 
in genome maintenance remains unclear. Here we report that C. elegans FANCD2 
(fcd-2) is dispensable for normal meiotic recombination but is required in 
crossover defective mutants to prevent illegitimate repair of meiotic breaks by 
nonhomologous end joining (NHEJ). In mitotic cells, we show that DNA repair 
defects of C. elegans fcd-2 mutants and FA-deficient human cells are 
significantly suppressed by eliminating NHEJ. Moreover, NHEJ factors are 
inappropriately recruited to sites of replication stress in the absence of 
FANCD2. Our findings are consistent with the interpretation that FA results from 
the promiscuous action of NHEJ during DNA repair. We propose that a critical 
function of the FA pathway is to channel lesions into accurate, as opposed to 
error-prone, repair pathways.