Whether it is by stabilizing HIF-1α to mediate the multiple drug resistance of breast cancer cells (96), or by promoting the localization of EGFR in the cell membrane, enhancing the EGFR signal to cause cancer cell proliferation (31), or by inhibiting the cell survival p38 MAPK pathway, inhibiting the activation of p53 transcription, and increasing the drug resistance of tumor cells to DNA damage drugs (43), it shows that the overexpression of AGR2 plays an important role in the treatment of breast cancer resistance. Here, TP53 is linked to neoplasm.