Objective To generate a Fancm gene knockout mouse model and to elucidate the biological functionof Fancm in mouse development. Methods Fancm ^{-/ -} mice were generated by the CRISPR/ Cas9 method. We analyzedtheir body weight, birth rate, gender ratio, and fertility. Blood samples were analyzed by a complete blood count (CBC).Testes from the Fancm ^{-/ -} and wildtype littermates were subjected to pathophysiological assessment. Results C57BL/6background Fancm knockout mice were generated by ATG region deletion using the CRISPR/ Cas9 method. Western blottingindicated the complete depletion of FANCM protein in the testis lysate from Fancm ^{-/ -} mice. The Fancm ^{-/ -} mice showed nosign of embryonic lethality. However, there were significantly less female Fancm ^{-/ -} mice compared with male Fancm ^{-/ -} mice.There was no significant difference in body weight between the Fancm ^{-/ -} mice and wild type littermates. The CBC indicateda slight, but significant, increase in the Hb level. The Fancm ^{-/ -} mice were infertile. The male Fancm ^{-/ -} mice had a reducedtesticular size and abnormal testicular architecture. The IHC and TUNEL assays indicated increases in cell cycle arrest andapoptosis in spermatogenic cells. Conclusions Fancm gene knockout causes defects of male reproductive organ development in mice.