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About 10–15% of non-obstructive azoospermia (NOA) patients show <em>AZFc</em> microdeletion in their blood leukocytes. However, if <em>AZF</em> genes were involved in impaired spermatogenesis, a higher frequency of chromosomal microdeletions was expected. In this study the frequency of <em>AZFc</em> microdeletion was compared with <em>TTY2</em> gene family, i.e., <em>TTY2A2A</em> and <em>TTY2A12A</em> in blood leukocytes of NOA patients and normal fertile control. In the present study 30 normal fertile individuals with mean age of 35.0 ± 6.0 and 30 NOA patients with mean age of 34.0 ± 7.0 were screened for microdeletion of <em>TTY2L2A</em> and <em>TTY2L12A</em> at Yq11 and Yp11 respectively and sequence-tagged site (STS) markers for <em>AZFc</em> gene using multiplex PCR technique. At the first step karyotyping was done for all subjects using standard G-banding technique to identify patients with normal karyotype as well as non-affected normal controls for molecular analysis.<br /> Results showed no <em>AZFc</em> microdeletion in normal and NAO patients whereas one <em>TTY2L2A</em> microdeletion in normal control (3.3%) and 4 in NOA (13.3%) was observed (<em>p</em> &lt; 0.05). However our data indicated that 6 of 30 NOA patients (20%) showed <em>TTY2L12A</em> microdeletion whereas there was no observed microdeletion in normal control (<em>p</em> &lt; 0.01).<br /> Results indicate that the studied genes might be involved in impaired spermatogenesis more effective than the routinely screened <em>AZF</em> genes in infertile men. Therefore, screening these genes along with <em>AZF</em> genes might be valuable for infertile patients. The reason why these genes are deleted from Y chromosome is not known but might be associated with genomic instability induced by environmental physico-chemical genotoxic agents.