Through the sequential SUMOylation and ubiquitination, misfolded proteins in cancer cells are efficiently degraded via the proteasome (Guo et al., 2014); furthermore, the capacity of TRIM19 to mediate the degradation of Atxn1-82Q protein aggregates in differentiated acute promyelocytic leukemia (APL) cells was found to be markedly reduced (Chen et al., 2017). Here, ATXN1 is linked to acute promyelocytic leukemia.