Although a potential strategy to target this repair downregulation has not yet been extensively explored, the Hung lab have built upon their work combining MET inhibitors with PARPi (see above) to demonstrate that EGFR cooperates with MET in subsets of hepatocellular cancers [148] and TNBCs [149] to phosphorylate PARP1 Tyr907 in response to DNA damage, demonstrating that dual EGFR/MET inhibition is required in this group to block phosphorylation and sensitize resistant cells to PARPi. This evidence concerns the gene MET and hepatocellular carcinoma.