Eight pathogenic races, determined based on the virulence displayed on differential chickpea culti-vars, have been recognized in Fusarium oxysporum f. sp. ciceris, the causal agent of Fusarium wilt of chick-pea. In order to elucidate the genetic relationships be-tween these races and understand how virulence evolved, we analyzed the sequences of 32 genomic regions for each of the eight races. Twelve of these regions were newly-designed microsatellite markers polymorphic for the F. oxysporum complex (10 displaying polymorphisms in the number of core re-peats, and two displaying polymorphic nucleotides in the microsatellite flanking regions), developed from a microsatellite enriched genomic library. The translation elongation factor 1-α (TEF), internal transcribed spacer region of the rDNA (ITS), five mitochondrial regions, a xylanase gene (xyl4) and its transcriptional activator (xlnR), two F. oxysporum f. sp. ciceris sequence charac-terized amplified regions (SCAR) and 11 microsatellites were completely identical for all races. Only a few polymorphisms were observed between and sometimes within races for the β-tubulin gene, intergenic spacer of the ribosomal DNA (IGS), endopolygalacturonase pg1 and exopolygalacturonase pgx4 genes, and six micro-satellite regions (four loci with repeat number variations and two loci with polymorphisms in flanking regions). In a previous study, race 3 of F. oxysporum f. sp. ciceris was reported to be Fusarium proliferatum based on TEF data of one isolate. However, our sequence analyses using TEF and other regions showed that the race 3 isolates in our study belong to F. oxysporum. The high degree of similarity among races supports a monophy-letic origin of this forma specialis and a subsequent development of pathogenic races within the lineage.