We demonstrated that by reducing the levels of miR-361, NEAT1 performed crucial roles in accelerating several critical steps of metastasis, including proliferation, invasion and cancer stemness-related property acquisition (such as self-renewal and drug resistance) and indirectly increased the expression of miR-361 target genes with known functions in forming of the premetastatic niche characterized by increased angiogenesis and inflammation [32]. The gene discussed is NEAT1; the disease is cancer.