This complements results of previous studies showing that NR4A1 coactivated Sp1 or Sp4, but not Sp3, and in these studies the CDIM-derived NR4A ligands act as inverse agonists to inhibit NR4A1/Sp1:Sp4-mediated expression of PD-L1, PAX3-FOX01, G9a, β1- and several other integrins in cancer cell lines [20, 39–45]. This evidence concerns the gene EHMT2 and cancer.