PRKG1 and seminoma: Bouskine et al. (2009) demonstrated that low concentrations of BPA promote proliferation in JKT-1 human seminoma cells by activating PKA and PKG via a membrane GPCR. However, in our study, membrane GPCR, EFGR-ERK, and PKG pathways participated in the proliferation of GC-1 cells stimulated by BPA. Transactivation of the EGFR and the ERK/MAPK cascade promoted by the GPCR agonist has been shown in a variety of cellular contexts. Again, estrogenic activation of the ERK/CREB pathway via a GPCR has already been demonstrated in several models (Belcher et al. 2005; Filardo 2002).