Could gap suppressing drugs help patients with FA?

**Figure 4 legend:** Suppressing the gaps to improve FA patient health. If gaps are the fundamental problem in FA, not failed repair of interstrand crosslinks as often proposed, drugs suppressing gaps could be improve FA patient health

Fanconi anemia (FA) is caused by mutations in one of at least 23 FA complementation (FANC) group genes. FA patients display congenital anomalies, hematopoietic stem cell (HSC) injury with increases bone marrow failure and leukemia, and high risk of secondary cancers. The most common feature of cells with FA gene mutations is sensitivity to drugs making DNA interstrand cross links (ICLs) propelling many studies into how FA proteins repair ICLs. However, it is not clear that failed ICL repair underlies FA phenotypes. Indeed, FA cells also have an underlying replication gap problem. Could suppression of gaps alone improve the fitness of FA cells or the health of FA patients? With this hypothesis in mind, we are screening for compounds that suppress gaps. This work is important because mutations underlying FA affect every cell in the body and there is currently no cure for FA.