So far, there are several pathways by which oncogenic KRAS may induce chemoresistance: first, it activates the RAF/MEK/ERK pathway; secondly, KRAS mutation induces COX-2 expression which heightens cancer cell binding to extracellular matrix and secrets more PGE2 to facilitate cell migration and dissemination; thirdly, KRAS mutation may activate the transcription of cellular protective stress response gene nuclear factor erythroid-derived 2 (NRF2) to protect against oxidative damage and promote drug resistance [56–58]. Here, KRAS is linked to cancer.