Fanconi anemia (FA) is an inherited chromosomal recessive syndrome characterized 
by cellular hypersensitivity to DNA crosslinking agents and bone marrow failure, 
which cause aplastic anemia, and an increased incidence of malignancy. 13 
complementation groups are currently discovered, and 13 distinct genes have been 
cloned (FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, FNACI, FANCJ, 
FANCL, FANCM, FANCN). Stem cells can theoretically divide to other cells without 
limit as long as a person is still alive. The stem cells that form blood and 
immune cells are known as hematopoietic stem cells. Hematopoietic stem cells can 
be acquired from a Fanconi anemia patient, whereas genomic DNA can be obtained 
easily from blood cells of a normal person. Normal genes also can be synthesised 
by PCR method. Normal genomic DNA will be delivered into a patient's stem cells 
via microinjection or transfection after enzyme digestion; the defective genes 
might be repaired by homologous genetic recombination. The gene-corrected stem 
cells can be transplanted into the same patient finally. It is possible that 
human genomic DNA to be considered as materials for homologous genetic 
recombination to repair defective genes in vivo. This might be an efficient 
method for gene therapy, which has no or less immunological rejection for 
Fanconi anemia and some genetic diseases. Several related observations and 
experiments are discussed to support this possible means of stem cell gene 
therapy of Fanconi anemia.