The results from the present and previous studies suggest that bacterial infection has the potential to increase fetal accumulation of P-gp substrates (cytokines, chemokines, endogenous and synthetic glucocorticoids, antibiotics, antiretrovirals, etc.; Bloise et al., 2016) both in earlier stages of pregnancy due to impaired placental P-gp activity (Bloise et al., 2013) and in later stages of pregnancy by decreasing labyrinthine-P-gp expression. The gene discussed is PGP; the disease is bacterial infectious disease.