Recent studies suggested an important role of other targets of SPOP as mediators of the oncogenic effects of the mutated SPOP. In fact, Geng and coworkers showed that SPOP-WT can physically interact with c-MYC protein and can promote c-MYC ubiquitination and degradation; this function is attenuated in SPOP-mutants, thus promoting c-MYC accumulation and promotion of prostate cancer cell proliferation [128]. This evidence concerns the gene MYC and prostate cancer.