To provide further proof-of-concept, we examined a panel of human colon cancer cell lines and noted that SW480 and SW48 cells provided the best evidence for an inverse association between miR-206 and KLF4. In cells with intermediate constitutive levels, forced expression or knockdown of miR-206 resulted in the expected reciprocal changes in KLF4, and miR-206 ectopic upregulation increased cell proliferation kinetics in real-time monitoring assays. The gene discussed is KLF4; the disease is colonic neoplasm.