We hypothesized that the oncogenic transcript of ERBB2 is stabilized on the 3’UTR with poly U sequence and that if the stabilizing element is destabilized, we could overwrite/outcompete the endogenous ERBB2-encoded message, degrade the ERBB2 transcript and protein expression, and thus control the aggressiveness of ERBB2+-driven cancers both in wildtype and drug-resistant settings. This evidence concerns the gene ERBB2 and cancer.