Therefore, we hypothesized that MEIS1 works as a transcription factor that mediates IPM genes and that, with methylated, MEIS1 was downregulated, which could not thoroughly stimulate the expression of favored IPM genes (SLIT2 and CLU), while that releases the expression of unfavored IPM gene (CDKN2A), thereby contributing to the initiation, development, and progression of colon cancer and worse prognosis. This evidence concerns the gene SLIT2 and colonic neoplasm.