“…In addition to Tex2, knockout of Tex33, Tex36, or Tex37 also leaves fertility unaffected, supporting that the functional compensation effect in the Tex gene family [30,31]. Indeed, several genes, including Tex11, Tex12, Tex14, Tex15, Tex17, Tex18 and Tex40, are essential in spermatogenesis, and deletion of which results in mouse infertility or subfertility, respectively [32,33]. Therefore, these genes play a crucial role in spermatogenesis, thereby compensating for the absence of certain genes, such as Tex2, and enabling knockout mice to maintain normal fertility.…”