Extending the findings of our previous study [16] we demonstrate that 1) G-1 increases intracellular ROS production in ACC cells, 2) ROS increases Egr-1 mRNA and protein expression most probably trough the activation of ERK1/2 signaling, 3) the increased expression and activation of Egr-1 causes a marked up-regulation of its target genes such as the pro-apoptotic factor BAX and the cell cycle inhibitor p21Waf1/Cip1 responsible for the inhibitory effect exerted by G-1 on ACC cells. Here, EGR1 is linked to adrenal cortex carcinoma.