Some cancers arise from novel proteins that are generated from aberrant fusion between genes that occurs during chromosomal translocations. For instance, FUS-CHOP, a fusion protein comprising the RNA-binding protein FUS and the stress-induced transcription factor CHOP, causes myoxid liposarcoma (MLS) by inducing transcriptional reprogramming, but the underlying mechanisms are unclear. Because FUS is known to undergo liquid–liquid phase separation (LLPS), and LLPS at super enhancers (SEs) has been suggested to control gene expression, Frank Shewmaker and colleagues (Owen et al., 2021) now investigate whether FUS-CHOP undergoes LLPS in vitro and in cells. They show that FUS-CHOP can indeed form condensates in vitro and that ectopically expressed FUS-CHOP undergoes LLPS in the nucleus of NIH 3T3 cells. Furthermore, in patient-derived MLS cells, FUS-CHOP is found in small nuclear puncta that colocalise with BRD4, a marker of SE condensates. Finally, ectopic expression using deletion constructs suggests that the interaction between FUS-CHOP and BRD4 is governed by the intrinsically disordered region (IDR) of FUS, suggesting that FUS-CHOP could drive condensate formation at certain SEs, thereby inducing an oncogenic transformation programme. Taken together, this work presents a novel mechanism of oncogenesis based on LLPS that might also be utilised to therapeutically target MLS and other cancers that are caused by IDR-containing fusion proteins.