For instance, in normal chondrocytic CFK2 cells and M12 prostate tumor cells, SOX9 overexpression resulted in decreased proliferation rate and cell cycle arrest in G0/G1 (3,4), while Sox9 knockdown in rat mesenchymal stem cells (MSCs) resulted in a marked decrease in proliferation rate through delayed S-phase progression and increased nuclear localization of p21 (5). Here, SOX9 is linked to prostate neoplasm.