KRAS and lung carcinoma: In vitro experimental model systems for miRNA alterations mediated by cigarette smoking in normal human bronchial epithelial and lung cancer cells derived from smokers and nonsmokers have demonstrated the repression of miR-487b, which leads to the upregulation of suppressor of zest 12 (SUZ12), B cell-specific Moloney murine leukemia virus insertion site 1 (BMI1), wingless-type family member 5A (WNT5A), MYC, and KRAS, thereby increasing cell proliferation, invasion, tumorigenicity, and metastatic potential of lung cancer cells in the cigarette-smoking group [14].