Ironically, a meta‐analysis of numerous cancer cell types identified DDIT4 as being overexpressed compared with non‐cancerous cells and associated with poor survival outcomes despite being a potent mTOR inhibitor.(23) Based on our findings from MG‐63 cells, we propose that 1,25(OH)2D may suppress tumor progression of other cancer types that involves mitochondrial‐to‐cytoplasmic DDIT4/REDD1 exchange. This evidence concerns the gene DDIT4 and neoplasm.