Moreover, luciferase assay revealed that upregulating miR-210-3p repressed, while silencing miR-210-3p elevated the reporter activity driven by the 3’UTRs of SOCS1 and TNIP1, but not by the mutant 3’UTR of SOCS1 and TNIP1 within the miR-210-3p–binding seed regions in PCa cells (Fig. 5e and f and Additional file 8: Fig. S4d). The gene discussed is TNIP1; the disease is posterior cortical atrophy.