Deregulated expression of MYC proteins is a major driver of human tumorigenesis and many tumors depend on high MYC expression throughout their lifetime, making it a prime target for therapeutic intervention. The canonical view postulates that MYC proteins are oncogenic transcription factors since they establish and maintain tumour-specific gene expression profiles. Our recent work identifies a number of potentially oncogenic functions of MYC that are independent of specific target genes: for example, we have found complexes of MYC that co-ordinate transcription with double-strand break repair at promoters and co-ordinate transcription with DNA replication. These findings not only shed new light on MYC function, but also open new opportunities to target critical MYC functions in tumorigenesis and I will discuss both aspects of our work.