Indeed, hsa-miR-5096 ectopic overexpression in PanNET insulinoma NT-3 cells led to a significant decrease of SSTR2 transcripts, while hsa-miR-5096 inhibition significantly boosted SSTR2 expression both in QGP-1 and NT-3 substantiating direct targeting and regulation in PanNETs characterized by SSTR2low/hsa-miR-5096high phenotype. The gene discussed is SSTR2; the disease is pancreatic insulinoma.