Thus like its mammalian counterpart FIR, Hfp behaves as a tumor suppressor to repress dMyc, which suggests that the mechanism proposed for transcriptional repression of c-Myc by FIR is conserved in Drosophila. These data suggest that the loss-of-function FIR mutants described in colorectal cancer may be sufficient to increase Myc expression, which would be predicted to lead to cancer initiation and progression. Here, MYC is linked to colorectal cancer.