Together, these data indicate that, in contrast to the human situation, but in line with studies in the mouse, bi-allelic inactivation of the rb1 gene is insufficient for retinoblastoma development in Xenopus. Although the efficiencies of gene disruption were relatively low, we believe that if rb1 bi-allelic mutation was sufficient to initiate tumorigenesis, tumors would have been detected. Here, RB1 is linked to retinoblastoma.