KEAP1 and non-small cell lung carcinoma: The presence of genetic and epigenetic abnormalities in this pathway, such as point mutations in functional domains of KEAP1 and NFE2L2 and methylation at the KEAP1 promoter region, was firstly described in NSCLC and then widely reported in many solid tumors, with the hypothesis that the lack of KEAP1 transcription induced high NRF2 activity and aberrant overexpression of ARE-driven target genes [6,10,16,18].