MiR-205 also participates in the cell proliferation of ER+/PR+ breast cancer; in fact, studies have demonstrated that angiomotin (AMOT), an adaptor protein regulating tight junctions, activates the ERK1/2 pathway to drive cell proliferation in ER+ breast cancer, and that miR-205 interferes with this mechanism by directly targeting AMOT in MCF7 cells [21,39]. This evidence concerns the gene AMOT and breast cancer.