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0 reviewsAlthough cancer initiation and progression are generally associated with the Open accessaccumulation of somatic mutations1,2, substantial epigenomic alterations underlie Check for updatesmany aspects of tumorigenesis and cancer susceptibility3–6, suggesting that genetic mechanisms might not be the only drivers of malignant transformation7. However, whether purely non-genetic mechanisms are sufcient to initiate tumorigenesis irrespective of mutations has been unknown. Here, we show that a transient perturbation of transcriptional silencing mediated by Polycomb group proteins is sufcient to induce an irreversible switch to a cancer cell fate in Drosophila. This is linked to the irreversible derepression of genes that can drive tumorigenesis, including members of the JAK–STAT signalling pathway and zf1, the fy homologue of the ZEB1 oncogene, whose aberrant activation is required for Polycomb perturbationinduced tumorigenesis. These data show that a reversible depletion of Polycomb proteins can induce cancer in the absence of driver mutations, suggesting that tumours can emerge through epigenetic dysregulation leading to inheritance of altered cell fates.