Functional assays by Liang Liu et al. have suggested that upregulated SNHG3 led to growth of cell proliferation, cell cycle progress and decrease of cell apoptosis, indicating that SNHG3 served as an oncogene in lung cancer by controlling tRNA processing, transcription, apoptosis, cell adhesion and signal transduction [22]. The gene discussed is SNHG3; the disease is lung carcinoma.