CDK4 and non-small cell lung carcinoma: PRMT6 can also interact with p16, overexpression of PRMT6 can counteract the cell cycle arrest at G1 phase caused by p16 in NSCLC A549 cells and decrease the association intensity of p16-CDK4, suggesting that PRMT6 probably achieves its cell apoptosis restraint role in NSCLC through p16 arginine methylation and provide a new idea for NSCLC treatment (78).