TMPRSS2-ERG rearrangement occurs in approximately 50% of prostate cancers and is associated with an aggressive phenotype (1,2). Both the TMPRSS2 and ERG genes resides on chromosome 21, and gene rearrangements involving the TMPRSS2 and ERG genes lead to the formation of a TMPRSS2-ERG gene fusion product (1,2). ERG is the most commonly overexpressed proto-oncogene in prostate cancer (1). TMPRSS2 is an androgen regulated gene, whose androgen response elements are believed to regulate ERG gene overexpression in TMPRSS2-ERG fusion positive samples (3). It has been well documented that TMPRSS2-ERG gene fusion is the result of the 5’ untranslated region of the TMPRSS2 gene (21q22) fusing with the 3’ coding region of the ERG gene (21q22) (4). Conventional cytogenetic testing utilizing fluorescence in situ hybridization (FISH) is considered the gold standard in detecting gene fusion rearrangements (4). The TMPRSS2/ ERG del- TECT (4 Color) FISH probe detects the gene fusion between the TMPRSS2 and ERG genes. Moreover, the novel multi-probe design allows for the detection of microdeletions that occur between the TMPRSS2 and ERG genes, which are associated with gene fusion events on chromosome 21 (5).