As far back as 1998, an animal study performed by Lankas GR et al.[17]had found that fetuses deficient in Abcb1 (-/-) were 100% susceptible to cleft palate resulting from exposure to avermectin, a known teratogenic substrate of P-gp, whereas the heterozygotes (-/+) littermates were less sensitive and the homozygous (+/+) fetuses with abundant P-gp were totally protected from the effects of teratogens. The gene discussed is PGP; the disease is cleft palate.