In lung cancer (LC), protein arginine methyltransferase 5 (PRMT5) was found to be overexpressed and to repress transcription of the miR-99 family by symmetrical dimethylation of histone H4R3, which increased fibroblast growth factor receptor 3 (FGFR3) expression, activated ERK1/2 and AKT, and in turn facilitated cell proliferation and metastases [93] (Table 1). Here, PRMT5 is linked to laryngotracheoesophageal cleft.