In contrast to in vitro studies that reported the resistance of d16HER2–expressing cells to the effects of trastuzumab, Alajati et al. showed that trastuzumab, administered in vivo to mice that had been xenografted with MCF10A cells that ectopically expressed d16HER2, blocked tumor growth [38], constituting the first evidence that the growth of tumor cells that are addicted to HER2 signaling can be blocked by anti-HER2 agents, even if the oncogene is primarily expressed as the d16HER2 splice isoform. Here, ERBB2 is linked to neoplasm.