The following observations demonstrate that ROS signaling mediates hERG misfolding resulting in defective trafficking: a) ROS levels were elevated in CH exposed neuroblastoma cells as evidenced by increased DCFDA staining as well as decreased aconitase activity in the cytosolic and membrane fractions, b) MnTmPyP, a membrane permeable ROS scavenger prevented CH-induced ROS generation as well as hERG degradation by restoring proper folding of the ER form and its interaction with Hsp90 leading to cell surface expression. This evidence concerns the gene KCNH2 and neuroblastoma.