Thus, we analyzed the tumor suppressive role of atrx in zebrafish that already harbored inactivating mutations of p53 and nf1. Homozygous deletion of atrx was lethal in developing fish, whereas the partial loss of this gene (atrx+/-) within the p53/nf1-deficient background led to a diverse spectrum of tumors not observed in animals that were wildtype for atrx, including epithelioid sarcoma, angiosarcoma, and rare carcinomas. This evidence concerns the gene TP53 and angiosarcoma.