Although a wealth of literature has supported the essential biological functions of PRMT5 in targeting histones [11, 14, 18], including symmetric dimethylation of histones H2A and H4 on R3 or histone H3 on R8 and asymmetric methylation of H3 on R2, the exact type of histone arginine methylation mediated by SHARPIN-PRMT5 in lung cancer metastasis is still unknown. Here, SHARPIN is linked to lung carcinoma.