Our study, based on the multi‐omics data from the TCGA database, integrated the clinical data and expression profiles, comprehensively analyzed the differences in clinical features, somatic nucleotide variations, gene expression, transcriptome, and tumor immune microenvironment between the KEAP1/NFE2L2/CUL3 pathway mutant and the wild‐type patients in LUAD. Here, CUL3 is linked to neoplasm.