In the present study, a relative decay in circulating anti-HER2 T-bet+IFN-γ+ (i.e., Th1), but not GATA-3+IFN-γ+ (i.e., Th2), phenotypes is associated with persistence of HER2pos tumors following neoadjuvant T + C. Taken together, these data suggest that abrogation of immunologic, particularly anti-HER2 Th1 function, may represent a HER2pos tumor-driven mechanism to evade immune surveillance during T + C treatment. Here, ERBB2 is linked to neoplasm.