Although METTL17 did not itself impact growth in K562 cells, it was nonetheless identified in our ATP screen performed in K562 human leukemia cells; these subsequent studies link METTL17 to a cancer-relevant endpoint in a different cancer cell line—in this case, human lung cancer cells—in which stable silencing of METTL17 significantly suppresses basal cancer cell proliferation without producing increased apoptosis. This evidence concerns the gene METTL17 and lung carcinoma.