Yu et al. (2014) observed that GPER was not only highly expressed in TNBC but was also involved in the activation of estrogen-mediated non-genomic ERK signaling. Based on clinicopathological evidence, p-ERK1/2 was detected in more than three-quarters of the GPER-positive TNBC specimens. Furthermore, high levels of GPER and p-ERK1/2 have been found to be prevalent in patients with a positive lymph nodes, large tumor size, and particularly an advanced clinical stage (Yu et al., 2014). The gene discussed is MAPK3; the disease is neoplasm.