Given that HER2 amplification/overexpression also occurs frequently in gastroesophageal cancers [15], and considering that some cancer patients can experience drug resistance to diverse available anti-HER2-targeted therapies (antibodies like trastuzumab, pertuzumab, T-DM1; tyrosine kinase inhibitors (TKI) such as lapatinib neratinib or tucatinib) [16], we proposed that identifying the functional mechanisms by which GSDMB over-expression modulates the therapeutic response of different HER2 tumors could have novel clinical utility. Here, ERBB2 is linked to cancer.