CCL4 and neoplasm: In this context, the activation of β-catenin in tumors inhibits the production of CCL4 by upregulating the transcription repressor ATF3, thus restricting the migration of conventional cDC1 towards the tumor, suggesting that tumors avoid immune surveillance by disrupting chemokine functionality.45,375 PGE2 diminishes the activity of NK cells, hindering their capability to produce inflammatory chemokines.