They observed that, in cultured breast cancer cells, treatment with G-1 decreased the expression of cyclin B, induced the arrest of the cell cycle in the G2/M phase, and caused apoptosis related to mitochondria, concluding that the activation of GPER can inhibit proliferation in vitro and in vivo through the generation of reactive oxygen species (ROS), apoptosis through the caspase pathway, and the decrease in cyclin B expression (67). Here, GPER1 is linked to breast cancer.