SLX4 and leukemia: Though functional validation studies are required to substantiate the role of these variants in hyperdiploid pre-B childhood ALL, our data suggest that concomitant inheritance of rare variants in FA genes FANCA, FANCP/SLX4, in combination with rare mutations in the endonuclease GEN1 and the meiotic recombination gene PRDM9, could lead to increased DNA damage and genomic instability, and thus contribute to hyperdiploid leukemia predisposition.