The transcription factors c-Myc and E2F are involved in regulating cell cycle progression. Overexpression of c-Myc in certain cell types induces noncycling cells to enter the cell cycle via a mechanism involving E2F-1 (1). E2F-1 is thought to regulate c-Myc expression via interactions with the retinoblastoma protein (2). TRRAP (for transformation/transcription domain-associated protein) interacts specifically with both c-Myc and E2F-1. Expression of trans-activated mutant TRRAP inhibits the oncogenic transformation of both c-Myc and E2F-1, suggesting that TRRAP is required for these oncogenic transcription factor pathways (3). TRRAP shares homology with the ATM/PI 3-kinase family, and it is highly conserved in evolution (4,5).