JAK2 and neoplasm: Notably, STAT3 activation—known to upregulate VEGF, MMP2, and PLK1—was significantly increased in LCN2-overexpressing tumor cells.30–32 While a previous study by Huang et al.27 showed that LCN2 binding to SLC22A17 activates JAK2–STAT3 signaling to drive CXCL1 expression, our findings demonstrate that in brain tumor cells expressing SLC22A17, LCN2 binding similarly activates JAK2–STAT3 but leads instead to VEGF-A upregulation.