To our knowledge, the current study is the first to identify that MALAT1 is aberrantly overexpressed in RP and that knockdown of MALAT1 greatly suppresses the osteogenic phenotype of hRIFs by targeting the miR-320a-5p/Runx2 axis in vitro, indicating the critical role played by MALAT1 in osteogenic differentiation of hRIFs through posttranscriptional mechanisms. The gene discussed is RUNX2; the disease is retinitis pigmentosa 1.