Treatment with the DPP-4 inhibitor KR62436 (KR) increased CXCR4, mTOR phosphorylation, HIF-1α, and LC3II, and decreased the levels of p62 in the human MCF7 and MDA-MB-231 breast cancer cell lines (Figure 2A); however, cotreatment with the CXCR4 inhibitor AMD3100 (AMD) abolished KR-induced phenotypes, such as mTOR phosphorylation, HIF-1α accumulation, and autophagic activation (Figure 2A). This evidence concerns the gene CXCR4 and breast cancer.