PCAT6 overexpression further induced the Akt/mTOR pathway by absorbing miR-4723-5p to elevate vascular endothelial growth factor receptor 2 (VEGFR2) levels, which in turn promoted triple-negative breast cancer (TNBC) cell proliferation, migration, invasion, and angiogenesis in vitro, as well as tumor growth, metastasis, and angiogenesis in vivo [26].Shi et al., also proved that PCAT6 increased the expression of tumor protein D52 (TPD52) by interacting with miR-185-5p in TNBC [27]. The gene discussed is AKT1; the disease is neoplasm.