We discovered that there are unique sequences on the poly U-rich elements (ARE) of the 3'UTR of mRNA that makes oncogenic HER2 transcript stable (15–17), and thus we engineered these elements to unstable forms and degraded HER2 across many HER2-driven cancer cell types both in wild-type and drug-resistant cancer models, which reduced primary tumor growth and inhibited metastasis (liver and lungs) in vivo in EGFRT790M HER2-positive osimertinib/trastuzumab-resistant NSCLC. The gene discussed is ERBB2; the disease is neoplasm.