Our findings are supported by orthogonal evidence: BioGRID database analysis confirms PRMT1‐vimentin interactions via affinity purification‐MS,[44, 45] and prior proteomic studies have implicated vimentin as a PRMT1 substrate.[46] In contrast to PRMT5‐mediated symmetric di‐methylation (sDMA) of vimentin at R196/R207/R345/R364 in MTAP‐deficient lung cancer,[13] our mass spectrometry analyses detected no dimethylation at these residues under hypoxic conditions, with only mono‐methylation (MMA) observed at R196. This evidence concerns the gene VIM and lung carcinoma.