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MFN1 (Mitofusin 1) and MFN2 (Mitofusin 2) are GTPases essential for mitochondrial fusion. Published studies revealed crucial roles of both Mitofusins during embryonic development. Despite the unique mitochondrial organization in sperm flagella, the biological requirement in sperm development and functions remain undefined. Here, using sperm-specific Cre drivers, we show that either <i>Mfn1</i> or <i>Mfn2</i> knockout in haploid germ cells does not affect male fertility. The <i>Mfn1</i> and <i>Mfn2</i> double knockout mice were further analyzed. We found no differences in testis morphology and weight between <i>Mfn</i>-deficient mice and their wild-type littermate controls. Spermatogenesis was normal in <i>Mfn</i> double knockout mice, in which properly developed TRA98+ germ cells, SYCP3+ spermatocytes, and TNP1+ spermatids/spermatozoa were detected in seminiferous tubules, indicating that sperm formation was not disrupted upon MFN deficiency. Collectively, our findings reveal that both MFN1 and MFN2 are dispensable for sperm development and functions in mice.