Our previous studies have demonstrated that cigarette smoke modulates microRNA expression in normal respiratory epithelia and lung cancer cells; CEBP/β-mediated upregulation of host gene for miR-31 and epigenetic repression of miR-487b activate Wnt signaling and upregulate MYC, KRAS, EZH2, and SUZ12, thereby enhancing a stem-like phenotype in pulmonary carcinomas [31, 33]. The gene discussed is KRAS; the disease is lung carcinoma.