To investigate the correlation between autosomal DAZL (deleted in azoospermia-like,DAZL) gene mutation and male spermatogenesis disorders. We collected 50 cases of azoospermia and 98 cases of oligospermia from January 2008 to June 2009 in the Institute of Reproductive Research, Yiji Mountain Hospital, South Anhui Medical College, and 63 cases of normal spermatozoa who had given birth within five years as the control group. All the study subjects were Han Chinese population in southern Anhui province, and there was no statistically significant difference in age and age at marriage between the two groups (P>0.05). The five sex hormones (FSH,LH,T,E2,PRL) were measured in all the case groups, and the azoospermic patients were routinely investigated for chromosome karyotype analysis and testicular biopsy. After signing the informed consent, 2 ml of peripheral elbow vein blood was drawn from each patient, and genomic DNA was extracted with a blood genomic DNA extraction kit (centrifugal column type). 9 pairs of primers were designed using Primer5.0 software, and the whole DAZL exon sequence was amplified by PCR. the PCR products were sent to Welltec Genetics Corporation (Beijing) for sequencing. The sequencing results were analyzed by Seqman in DNASTAR software package, and MegAlign was used to compare with the standard sequences to find the mutation sites and compare and check them one by one. The data were analyzed with SPSS11.5 software. The mutation frequency was analyzed by χ2 test,and was statistically significant at ( P < 0. 05). One case was found in the azoospermia group in which the nucleotide of exon 2 SNP260 was changed from A to G and resulted in the change of codon threonine to alanine at position 12, whereas no change in T12A was found in the oligospermia group and the control group. Screening of other exons did not reveal any other mutation sites. This patient had been married for two years without pregnancy and had no family history of the disease. Sex hormone tests were slightly above normal for FSH and LH, slightly below normal for androgens, and within the normal range for PRL. No mature spermatozoa were found in the homogenate of testicular tissue biopsy, and the testicular tissue biopsy was sent to pathology, which returned the following results: microscopic examination of the varicocele lined with supportive cells, and a small number of spermatogonial cells were seen in the lumen, with no spermatogonial cells or mature spermatozoa seen.