Our data indicate that the oncoprotein HBXIP, functioned as a co-activator of NF-κB (p65) or PPARδ, transactivated the promoter activity of PPARδ or NF-κB, and enhanced the expression of PPARδ and NF-κB in mRNA and protein levels in a positive feedback loop manner, leading to the fast growth of colonic cancer cells. This evidence concerns the gene LAMTOR5 and colonic neoplasm.