Treatment of a Fanconi mouse model with metformin partially suppresses cancer predisposition and rescues HSC defects. Under conditions of stress, HSCs are recruited into active cell cycling, leading to altered metabolism with the production of additional ROS and potentially an increase in aldehyde production. Metformin may have a metabolic effect on HSCs to reduce the production of these toxic molecules. Metformin can also react with aldehydes, directly rendering them inert and acting as a scavenger for excess aldehydes. Metformin leads to decreased levels of DNA damage circumventing the need for an intact Fanconi DNA repair pathway.