In a previous study, we found Cd stimulated growth of human uterine leiomyoma cells at lower concentrations ≤ 20 μM and this effect was not mediated by a classical ER mechanism of receptor binding and ERE-mediated gene activation, but through nongenomic pathways involving G protein-coupled estrogen receptor 1 (GPER) and activation of Epidermal Growth Factor Receptor (EGFR), with subsequent MAPK/ERK1/2 phosphorylation (Gao et al. 2015; Liu et al. 2019). The gene discussed is MAPK3; the disease is Uterine leiomyoma.