Additionally, supraphysiological SOD3 expression in anaplastic cancer cells activates AKT-GSK3-β-catenin signaling but prevents β-catenin nuclear transfer by increasing the gene expression of WW domain-containing transcription regulator protein 1 (WWTR1), snail homolog 2 (SNAI2), and axis inhibition protein 2 (AXIN2) [75], which are responsible for β-catenin cytoplasmic arrest, binding, and degradation, respectively [81–83]. This evidence concerns the gene AXIN2 and anaplastic cancer.