Fibrolamellar carcinoma results from a genetic lesion that produces the DNAJ-PKAc fusion kinase, which is recruited into macromolecular complexes and is sensitive to combinations of signal transduction inhibitor drugs.

Protein kinase A-driven increases in c-MYC protein expression and tumor cell proliferation can be blocked by eIF4A inhibitors, suggesting a potential new treatment option for patients with oncogenic PKA activation.