In line with the studies above describing the tumor suppressive function of SPOP in CRC, Zhi et al. showed that SPOP accelerated the ubiquitination and degradation of Gli2 by directly binding and interacting with it in CRC cells, enhancing the apoptotic signals of cells via a decrease in Bcl-2 and blocking the progression of CRC [31]. The gene discussed is SPOP; the disease is neoplasm.