Previously, we demonstrated that Midnolin (MIDN) is a novel genetic risk factor for Parkinson‘s disease in Yamagata and British population by genome-wide association study. In PC12 cells, neurite outgrowth was completely blocked by Midn deletion by genome-editing. In this study, because we found that insulin promoted MIDN gene expression in SH-SY5Y human neuroblastoma cells, we attempted to clarify the mechanism in detail. MIDN expression was promoted accompanied by the activation of ERK1/2 and PI3-kinase. We also used a DNA construct encoding human MIDN promoter linked to firefly luciferase, and identified important regions on the MIDN promoter. The region (-121 bp~-99 bp) includes TFAP2 consensus sequences, MIDN promoter activity was enhanced by mutation at the sequences and overexpression of dominant-negative mutant of TFAP2. In contrast, the region (-71 bp~-57 bp) includes AP-1 consensus sequence, MIDN promoter activity was decreased by mutation at the sequence. Insulin promoted AP-1 activity accompanied by the expression of c-FOS, which was blocked by U0126 and wortmannin, an ERK1/2 and PI3-kinase inhibitor, respectively. MIDN promoter activity was decreased by decoy oligodeoxynucleotide for AP-1 and AP-1 inhibitor, SR11302. These results suggest that insulin promotes MIDN gene expression mediated through AP-1.