Most significantly, we found that the JIMT-1 cells responded to JNK inhibition when compared to the JIMT-1 cells treated with DMSO (Fig 1B), which we did not robustly observe in the BT474 cell line as the Caspase-3 activity induced in BT474 cells treated with JNK inhibitor was not statistically significant when compared to BT474 cells treated with DMSO (Fig 1A), suggesting that JNK signaling could play a role in regulating the survival of HER2+ breast cancer cells that are resistant to HER2 inhibitors. The gene discussed is CASP3; the disease is breast carcinoma.