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Fibrolamellar carcinoma (FLC) is a deadly liver cancer affecting adolescents and young adults without prior history of liver disease and lacks effective drug therapy. Several established histological and molecular features characterise FLC, including the presence of prominent fibrotic bands and the occurrence of a genetic fusion driver DNAJB1-PRKACA (DNAJ-PKAc).1 More recently, another entity was described; the FLC-like tumours, also presenting with activating PKA mutations and concomitant BAP1 mutations.2 Clearly, FLC(-like) tumours possess genetic aberrations of PKA signalling components; however, many open questions remain. For example, what is the exact oncogenic function of DNAJ-PKAc in FLC tumour growth? Which signalling networks are affected, and does this associate with targetable therapeutic vulnerabilities?