The steady state (7 day) Cmax for sorafenib is ~21 μM in plasma, with ~99% of the drug protein bound based on in vitro human serum binding assays; though it is known that the drug is also rapidly taken up into tissues, and in addition patient data from clinical trials would argue that a significant amount of the drug has to be bioavailable, at least in the low micro-molar range, in a tumor based on its single agent effects by decreasing both ERK1/2 phosphorylation and reducing MCL-1 protein expression in tumor cells that are not specifically oncogene addicted [12, 13]. Here, MAPK3 is linked to neoplasm.