Other studies have shown selective killing by PARP inhibition of cells from diverse tumor types bearing mutations in ATM, MRE11A, BRCA2, or the EWS-FLI1 translocation, suggesting that PARP is a bona fide hub for genetic interactions with cancer genes (Brenner et al. 2012; Bryant et al. 2005; Farmer et al. 2005; Vilar et al. 2011; Williamson et al. 2010). This evidence concerns the gene FLI1 and cancer.