The molecular mechanisms by which SMYD3 exerts its functions are attributed to epigenetic control of gene expression through the methylation of histones (H3K4, H4K5, and H4K20) [32,33,34], and the methylation of non-histone proteins, such as MAP3K2 (mitogen-activated protein kinase 2) [35] and VEGFR1 (vascular endothelial growth factor receptor 1) [36] in cancer development. Here, MAP3K2 is linked to cancer.