To further investigate the mechanism underlying the role of Parkin in tumor suppression, we searched for potential ubiquitination substrates of Parkin by screening for potential Parkin-interacting proteins using two sequential rounds of immunoprecipitation (IP) followed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) assays in MCF7 cells transduced with a pLPCX-Myc-Parkin vector to express Myc-Parkin or with the empty vector as a control. This evidence concerns the gene MYC and neoplasm.