MYC proto-oncogenes are deregulated in, and contribute causally to, a large proportion of human tumors. They function as transcription factors and as such are considered difficult to target pharmaceutically. Therefore, intense efforts have been directed at identifying MYC interaction partners that might lend themselves to pharmaceutical inhibition. I will describe the role of one such protein, SPT5, for MYC-dependent tumors in the model system Drosophila. In addition, I will touch on one aspect of transcription in vertebrate cells as well as a newly discovered transcription-independent function of vertebrate MYC proteins.