For example, considering the key role played by tMΦs-produced CSF1, if in vivo exposure to GEN-DEHP mixtures (or other EDCs with equivalent mechanism of action and molecular targets) inhibited the production of CSF1, disrupting its signaling on SSC-expressed CSF1R and altering the tyrosine kinases downstream of CSF1R, which could result in inadequate SSC pool, failure of spermatogenesis and infertility, as observed in ours and others animal studies of EDC exposures. The gene discussed is CSF1R; the disease is Infertility.