Toxicol. and phosphoinositide 3-kinase pathways. Fenhexamid activation was inhibited from the arylhydrocarbon receptor antagonist -napthoflavone. Fludioxonil and Fenhexamid didn’t affect dihydrotestosterone-induced miR-21 manifestation. Fludioxonil, however, not fenhexamid, inhibited MCF-7 cell viability, and both inhibited estradiol-induced cell proliferation and decreased cell