These results and the results presented therein thus confirm that in mice, the severity of the phenotype is dependent on Spink2 expression levels and that there is a phenotypic continuum ranging from (i) azoospermia in the complete absence of the protein (ii) to teratozoospermia and oligozoospermia associated with subfertility when only a fraction of the protein is present and finally (iii) to astheno‐teratozoospermia with no impact on fertility when half of the protein is present. The gene discussed is SPINK2; the disease is Abnormal sperm morphology.