Higher‐order SPOP oligomerization and multivalent interactions between SPOP and its substrates cooperatively trigger SPOP LLPS.[61, 206] Typical mutations in SPOP disrupt phase separation and DAXX ubiquitination in prostate cancer,[206] implying that defects in SPOP LLPS result in oncoprotein accumulation. The gene discussed is SPOP; the disease is prostate cancer.