This approach is exemplified by the observation that while Fancc‐/‐ mice do not develop bone marrow hypocellularity, the Fancc‐/‐ and Sod1‐/‐ double mutants develop this feature and go on to develop anemia and leucopenia, providing some evidence that oxidative stress contributes to bone marrow failure in FA 61. This evidence concerns the gene FANCC and anemia.