When miR-183 activity was increased, it upregulates BRI3, whose positive relationship correlates with p38/ERK/AKT and Wnt/β-catenin pathways, suggesting a complicated tumor-promoting mechanism which includes interaction among MEG3, miR-183, and BRI3 via p38/ERK/AKT and Wnt/β-catenin signaling [230,231]. The gene discussed is AKT1; the disease is neoplasm.