Fanconi anemia is a rare recessive disorder characterized by genome instability, 
congenital malformations, progressive bone marrow failure and predisposition to 
hematologic malignancies and solid tumors. At the cellular level, 
hypersensitivity to DNA interstrand crosslinks is the defining feature in 
Fanconi anemia. Mutations in thirteen distinct Fanconi anemia genes have been 
shown to interfere with the DNA-replication-dependent repair of lesions 
involving crosslinked DNA at stalled replication forks. Depletion of SLX4, which 
interacts with multiple nucleases and has been recently identified as a Holliday 
junction resolvase, results in increased sensitivity of the cells to DNA 
crosslinking agents. Here we report the identification of biallelic SLX4 
mutations in two individuals with typical clinical features of Fanconi anemia 
and show that the cellular defects in these individuals' cells are complemented 
by wildtype SLX4, demonstrating that biallelic mutations in SLX4 (renamed here 
as FANCP) cause a new subtype of Fanconi anemia, Fanconi anemia-P.