Dnah17–/– and Eno4–/– knockout mice demonstrate male infertility due to abnormal development of the axoneme and flagellar structures (Nakamura et al., 2013; Whitfield et al., 2019), while loss of Spem1 in Spem1–/– mice leads to sperm deformation and loss of motility due to aberrant removal of the cytoplasm during development and retention of excess residual cytoplasm in the cytoplasmic droplet (Zheng et al., 2007). This evidence concerns the gene SPEM1 and male infertility.