In these studies, the authors typically showed that siRNA-mediated knockdown of MALAT1 in cancer cell lines resulted in a certain phenotype, such as proliferation, migration, invasion, chemosensitivity, or radiosensitivity, followed by luciferase assays to demonstrate the existence of the miRNA-binding site on MALAT1. Then, functional experiments demonstrated that the miRNA and its target gene mediate the effect of MALAT1. While the ceRNA model is interesting and MALAT1 might function as a ceRNA under certain circumstances, more rigorous experiments are needed to prove this model. The gene discussed is MALAT1; the disease is cancer.