These include the tumor-suppressive let-7 that targets the KRAS transcript11; the APC-targeting miR-135 that triggers activation of WNT signaling and chromosomal instability12; the microsatellite instability-promoting miR-155 that downregulates the multiple mismatch repair genes MLH1, MSH2, and MSH613; and the DNA methyltransferase-inhibiting miR-29, miR-143, and miR-342, which collectively alter overall DNA methylome profiles and consequently contribute to misexpression of key tumor suppressors and oncogenes14–16. The gene discussed is KRAS; the disease is neoplasm.