Additionally, although DXS253E may offer an alternative opportunity to delay the progression of CRC, further investigation of its functions in vitro and in vivo is necessary to identify the molecular mechanism underlying DXS253E regulation of the tumor microenvironment, as well as the potential of AKT/mTOR-targeted treatment for CRC patients with high DXS253E expression. This evidence concerns the gene AKT1 and neoplasm.