Geng et al reported that SPOP mutants lost the ability to modulate SRC-3 and AR transcriptional activity.[24] A follow-up study also showed that SPOP mutation drove prostate tumorigenesis depending on coactivation of both SRC-3-mediated phosphatidylinositol-3 -kinase (PI3K)/mammalian target of rapamycin (mTOR) and AR signaling.[25] A study in 2018 by Zhang et al demonstrated that SPOP promotes the ubiquitin-mediated degradation of programmed death-ligand 1, a promising target for immunotherapy. The gene discussed is NCOA3; the disease is medical procedure.