This hypothesis is supported by the following observations: (1) MEG3 overexpression only partially rescued the promoted cell proliferation caused by POU3F3 overexpression, indicating the interaction between POU3F3 and other factors; and (2) expression levels of POU3F3 and MEG3 were significantly and inversely correlated in tumor tissues but not in normal tissues, indicating the existence of pathological mediators between POU3F3 and MEG3. The gene discussed is MEG3; the disease is neoplasm.