As introduced, PTMs critically influence HuR function,60,62–69 in addition to being currently considered attractive therapeutic targets in cancer.3 Together with our earlier discovery that neddylation stabilized HuR leading to its increased abundance in HCC,66 here we demonstrate that HuR SUMOylation may also contribute to liver tumor progression by affecting its intrinsic RNA-binding affinity, further modifying the transcriptomic profile. The gene discussed is ELAVL1; the disease is cancer.