Of note, we previously found a role for MLK3 in JNK-mediated phosphorylation of paxillin in MCF10A and TNBC cells.8 In MCF7 cells, we observe a modest increase in phospho-paxillin on MLK3 expression, which is unaffected by FRA-1-silencing (Supplementary Figure 6) suggesting that MLK3 regulation of paxillin is independent of FRA-1, and consistent with the idea that MLK3 controls multiple pathways in cancer cell migration and invasion. The gene discussed is FOSL1; the disease is cancer.