Depletion of PML in U2OS and HeLa cells resulted in loss of foci formation and mono-ubiquitination of FANCD2. Interestingly, we found that damage-induced CHK1 phosphorylation is severely impaired in cells depleted with PML. In addition, we showed that CHK1 plays a critical role in Fanconi anemia gene expression, demonstrating that PML regulates FA gene expression by promoting damage-induced CHK1 phosphorylation. This evidence concerns the gene PML and Fanconi anemia.