Based on the rapid response to HER2 blockade by trastuzumab in modulating CD36 in HER2 + BC observed in this trial —regardless of their tumor sensitivity to treatment—further research is warranted to clarify the functional role of the rapid increase in CD36 expression compared with the changes observed with long-term neoadjuvant anti-HER2 treatment, which we demonstrated to be associated with CD36-driven FA uptake and the emergence of a mesenchymal-like CSC phenotype promoting resistance. The gene discussed is CD36; the disease is neoplasm.