Mechanistic studies on the stable CD44 high cell line (ADR44P) revealed that the increased NRF2 content was caused by CD44-p62 signaling, while the genetic silencing of NRF2 was able to markedly suppress the aggressive phenotype of CSC, including drug resistance, colony/sphere formation and cell migration in vitro, but, also, tumor growth in vivo [40]. Here, NFE2L2 is linked to neoplasm.