In mice, deletion of various enzymatic subunits led to distinct phenotypical outcomes: Cnot4 deletion caused male infertility (Dai et al. 2021a, b); Cnot6 deletion had no obvious phenotypes (Mostafa et al. 2020), while Cnot6l deletion led to metabolic abnormalities (Dai et al. 2021a, b) and Cnot6/Cnot6l double deletion resulted in female infertility (Dai et al. 2021a, b); Cnot7 deletion also caused male infertility (Berthet et al. 2004); and Cnot8 deletion led to early embryonic lethality (Mostafa et al. 2020). This evidence concerns the gene CNOT6L and male infertility.