NR2C2 and neoplasm: As shown in Figure 3B, whereas MEK-162 treatment (20 and 40 μM for 72 h) inhibited proliferation of corticotroph tumor cells transfected with a nonsense control (Mean ± SE, proliferation FD, Vehicle: 1±0.001; MEK-162 20 μM: 0.4±0.004, p < 0.05; MEK-162 40 μM: 0.3±0.02, p < 0.05, Figure 3B), knockdown of TR4 attenuated the growth inhibitory effects of MEK-162 treatment (Mean ± SE, proliferation FD, Vehicle: 0.8±0.06; MEK-162 20 μM: 0.6±0.07, p < 0.05; MEK-162 40 μM: 0.4±0.03, p < 0.05, Figure 3B).