Transmissible cancers are malignant cells that transmit between individuals, akin to both a parasite and mobile graft. The mechanisms that allow these cancers to metastisise between individuals provide fundamental insights into the evolution of immune escape traits and competition dynamics between malignant and healthy cells more generally. The Tasmanian devil is threatened by the remarkable emergence of two independent lineages of transmissible cancer, devil facial tumour (DFT) 1 and devil facial tumour 2 (DFT2). In this talk I will describe the different mechanisms used by these cancers to escape the host immune response and how immune escape traits are evolving in response to pressure from the host. I will also discuss a recent analysis of the peptides presented by Major Histocompatibility Complex class I (MHC-I) molecules on transmissible cancer cells and healthy Tasmanian devil cells, which revealed that MHC-I allotypes expressed by transmissible cancer cells share a dominant motif with preference for a hydrophobic Leucine residue at position 3 and position W of peptides. These results suggest that polymorphisms in MHC-I molecules between tumours and host can be ‘hidden’ by a common peptide motif, providing the potential for permissive passage of infectious cells and demonstrating complexity in mammalian histocompatibility barriers.