Notably, there was no pattern of RNF5 abundance that either positively or negatively correlated with the presence of FLT3 or NPM1 mutations (Supplementary Fig. 1h, i), suggesting that the significance of RNF5 activity to AML may not depend on any specific oncogenic driver(s) or activation of particular signaling pathways. Here, FLT3 is linked to acute myeloid leukemia.