Our present results indicated that phosphorylated CSE1L is a secretory protein (Figure 1); vemurafenib and sorafenib treatment inhibited ERK1/2 and CSE1L phosphorylation (Figures 2, 3); and serum phospho-CSE1L levels declined 3–5 days after the administration of targeted drug therapies, namely vemurafenib and sunitinib treatment and sorafenib and lapatinib treatment, in tumor xenograft models (Figures 4, 5, 6, 7). This evidence concerns the gene MAPK3 and neoplasm.