Some repetitive sequences can undergo erroneous expansion during DNA replication, which may lead to neurodegeneration and other pathologies. Such expanded repeats can be aberrantly expressed in a process known as repeat-associated non-AUG (RAN) translation. Kearse et al. established a reporter assay to study the mechanism of RAN translation both in vitro and in cells. Focusing on CGG repeats, which are found in the FMR1 gene and can cause fragile X mental retardation, they showed that translation of repeats initiated at non-AUG codons, at least in part, shares a mechanism with canonical translation, involving 5′ cap-dependent scanning by ribosomes. They further revealed that RAN translation is influenced by the repeat length, the reading frame and the surrounding sequence, generating diverse protein products with variable efficiency. Analysis of other pathology-associated repeats should provide further insights into the features and mechanism of RAN translation.