Loss-of-function experiment demonstrated that silencing of SBF2-AS1 remarkably upregulated P21 expression, thus suppressing NSCLC cell proliferation, migration and invasion [26].Additionally, one study manifested that SBF2-AS1 and a disintegrin and metalloproteinase 17 (ADAM17) share a functional miR response element, miR-338-3p, and SBF2-AS1 ultimately accelerates NSCLC progression through the ceRNA network [50]. The gene discussed is ADAM17; the disease is non-small cell lung carcinoma.