Our data biologically explain the preclinical findings obtained by Feng and colleagues, who showed the advantage of concomitant inhibition of CD36 and HER2 over monotherapy in reducing tumor cell proliferation [11], and offer mechanistic support for the results of our previous clinical study describing the outcome of CD36+ HER2 + BC patients receiving neoadjuvant trastuzumab [13]. The gene discussed is ERBB2; the disease is neoplasm.