gWe employed an endpoint genotyping method to update the prevalence rate of positivity for the TR 34 /L98H mutation (a 34-bp tandem repeat mutation in the promoter region of the cyp51A gene in combination with a substitution at codon L98) and the TR 46 A zole resistance in Aspergillus fumigatus is a global and evolving public health threat which translates into treatment failure (1). Surveillance studies indicate that the incidence of azole resistance is increasing (2-6), with the TR 34 /L98H mutation (a 34-bp tandem repeat mutation in the promoter region of the cyp51A gene in combination with a substitution at codon L98) emerging in multiple European countries and in the Middle East, Asia, and Africa and with a new resistance mechanism, the TR 46 /Y121F/ T289A mutation (a 46-bp tandem repeat mutation in the promoter region of the cyp51A gene in combination with substitutions at codons Y121 and T289), emerging more recently in Europe and India (2-6). We also previously reported the occurrence of the TR 34 /L98H mutation in 3.2% of clinical Aspergillus fumigatus isolates obtained from patients in Iran to the end of 2009 (5).The trend of increases in the rates of azole resistance among A. fumigatus isolates in different regions and patient groups exemplifies the fact that knowledge of the (local) epidemiology of azoleresistant Aspergillus diseases is important for clinical mycology/ microbiology reference laboratories (7-9). Moreover, rapid and specific molecular methods for the identification of the recently identified azole-resistant A. fumigatus strains can significantly influence a timely decision on patient management (10).In our search for a novel, rapid, sensitive, accurate, and highthroughput method for detection and screening of azole resistance in A. fumigatus, we found that endpoint genotyping targeting a single-nucleotide polymorphism (SNP) in the cyp51A gene could provide an option. The quantitative analysis of SNPs has been a reliable method in diagnostic microbiology for identification of a single nucleotide in the genomes of humans (11-15), viruses (16-20), and bacteria (18). In this assay, an extension probe can be simply designed to anneal to the template in a posi-