Regional testicular factors or environmentally friendly or genetic background could be responsible for the phenotypic variability highlighted in previously reported instances. In particular, investigations of the Y haplotype in individuals holding a USP9Y deletion would be useful to determine whether there exists a correlation between genetic background and phenotypic variation. Based on the normal rate of USP9Y transcription in patients with spermatogenic failure and the absence of its correlation with the degree of sperm retrieval,16 we also infer that USP9Y has a marginal part or no function in spermatogenesis. Consistent with this hypothesis is the inactivation of the orthologous gene in chimpanzees and bonobos.17 In conclusion, we found that complete deletion of the USP9Y gene does not cause spermatogenic defects, nor does it preclude the organic conception of children.9 Our results indicate that USP9Y is not needed for normal sperm production and fertility in humans and that a revision of the diagnostic approach of screening for Y-chromosome microdeletions, according to EAA-EMQN guidelines,11 may be warranted.Compared with participants whose sleep length was unchanged, this change to an extended sleep duration was connected with lower scores at follow-up on five of six cognitive function tests, with the just exception being the test of short-term verbal memory. The sleep duration at follow-up around 25 % of ladies and 18 % of men had reduced from ‘6, 7, or 8 hours’ per night time at baseline. This change to a shorter rest duration was connected with lower ratings at follow-up on three of the six cognitive exams, with reasoning, vocabulary and global cognitive status all adversely getting affected. Surprisingly, an increase in sleep duration from six hours or much less showed no evidence of an advantageous effect.