Previously, we have shown that GSK3 activity regulates NRF2 by phosphorylating the DSGIS motif located within the Neh6 (NRF2-ECH homology 6) domain of NRF2, thus promoting proteasomal degradation directed by β-TrCP (beta-transducin repeat-containing protein)-CUL1, a mechanism that has been reported in human and mouse tumour cells [13,14]. This evidence concerns the gene BTRC and neoplasm.