Moreover, the phosphorylation level of HSP27 S15 and the nuclear translocation of HER2 and p-HSP27S15 were greatly reduced in tumor tissues excised from the TZMB + J2 group (Figure 8F,G), once again confirming the finding that downregulating the chaperone activity of HSP27 by inhibiting S15 phosphorylation could allow TZMB-refractory BC patients to obtain clinical benefit from TZMB, by reducing the stability of overexpressed HER2, and placing it in a pregnable state. The gene discussed is HSPB1; the disease is breast cancer.