To investigate the mechanism by which MEK1/2 inhibition cooperates with HDAC inhibition in TPM cancers, SNU475 (hepatocellular carcinoma) and LN229 (glioblastoma) cells were treated with clinically relevant MEK and HDAC inhibitors, including TR and VOR, along with other specific HDAC inhibitors: mocetinostat (MOC, HDAC 1/2/3 inhibitor, 1 μM), entinostat (ENT, HDAC 1/3 inhibitor, 2 μM), LMK235 (LMK, HDAC 4/5 inhibitor, 1 μM), and nexturastat (NEX, HDAC 6 inhibitor, 2 μM). This evidence concerns the gene MAP2K1 and glioblastoma.