Interestingly, the SPOP mutant subset of prostate cancers had some notable molecular features, including mutual exclusivity with ERG gene rearrangement, elevated levels of DNA methylation, homogeneous gene expression patterns, frequent deletion of CHD1 and overexpression of SPINK1 mRNA, supporting the concept that SPOP mutation tumors represent a distinct molecular subclass of prostate cancer [4] SPOP is one of the adaptor proteins of the CUL3-RBX1 E3 ubiquitin ligase complexes. Here, CHD1 is linked to prostate carcinoma.