Moreover, CRC patients with KRAS mutations have been shown to have an inferior response to most KRAS-targeted therapies, so the CRC consortium has suggested that a comprehensive understanding of molecular interactions in pathways is important for mutant CRC signaling in KRAS and that the integration of multi-omics data (genome, transcriptome, epigenome, metabolome, and immunome) can help to understand and propose the development of combination therapies with potential therapeutic use suitable for KRAS mutant CRC [7]. This evidence concerns the gene KRAS and colorectal carcinoma.