NFKB1 and neoplasm: By inhibiting NF-κB, TZD-activated PPARγ substantially lowers the expression of pro-inflammatory, pro-angiogenic, and pro-metastatic signaling molecules in CAFs, including IL-6, IL-8, CXCR4, MMP2, and MMP9, which further dampens pro-tumor crosstalk in the TME [117,118].