GPER is often overexpressed in seminomas but not in non-seminomas [58,59]; this overexpression tends to stimulate seminoma cell proliferation by activating ERK1/2 and protein kinase A. An in vitro analysis using JKT-1 cell lines (derived from a human testicular seminoma) revealed that the binding of endocrine disruptors (EDCs) such as bisphenol A (at a low concentration) to GPER induces seminoma cell proliferation [60,61]. The gene discussed is GPER1; the disease is testicular seminoma.