From these findings, the questions arise (1) whether the HRG rescue effect is relevant for all MET-amplified gastric cancer cells, (2) if alterations in HER receptor expression and/or signaling are observed upon MET inhibition, (3) whether HRG elicits its positive effects via HER1/HER3 or HER2/HER3-promoted survival signaling in this context, and (4) which other molecules are involved in MET resistance. Here, EGFR is linked to gastric cancer.