While the sheer number of genes with changing expression levels paralleling CHRM1 was high, the fact that the most concurrently downregulated pathways were CHRM1-related while the most concurrently upregulated GO terms were growth- and proliferation-related, implies the strong correlations were unlikely due to chance and reflect the impact of CHRM1 downregulation in colon cancer. This evidence concerns the gene CHRM1 and colonic neoplasm.