Oxidation of hepatocyte mitochondria due to iron overload led to hepatocyte injury, elevated TGF β and fibrosis. Fibrosis starts with stellate cell fibro genesis activated by chronic hepatocyte injury. Liver fibrosis is the main cause of morbidity and mortality in iron overload. Deferasirox is an iron chelation drug serving to bind iron overload and having ant fibrotic effect. To examine the effect of deferasirox on liver fibrosis prevention due to iron overload. This experimental research used post-test only control group design on male Balb/c mice that were randomly divided into 3 groups. Group 1 (NaCl+S) was administered with 0.3 cc Na Cl 0.9% through intra peritoneal (I.P) injection and drug solvent (Aquabidest, CMC and Nipagin) per oral (P.O) intermittently. Group 2 (Fe+S) was administered with 0.3 cc 1.5 mg Fe+sucrose (Venofer®) through I.P injection and drug solvent (Aquabidest, CMC and Nipagin) P.O intermittently. Group 3 (Fe+Dfx) 0.3 cc 1.5 mg Fe+sucrose (Venofer®) I.P injection, and Deferasirox 20 mg/kgBW/day P.O intermittently. All of the treatment was given for 60 days. Fibrosis area fraction of liver was assessed using software ImageJ. The average fibrosis area fraction of group 1 was 0.00 ± 0.00%, group 2 was 9.17 ± 8.54% and group 3 was 1.38 ± 0.20%. The fibrosis area fractions between group 2 and 3 were significantly different with p value 0.000 (p<0.05). The body weight of group 2 was higher than that of groups 3 and 1. Iron overload causes liver fibrosis in male Balb/c mice. Deferasirox administration may lower the area of liver fibrosis in male Balb/c mice due to iron overload.