To assess whether methylation of MAP3K2 at K260 drives aggressive properties of PCa cells linked to high levels of SMYD3 expression, we tested cancer cell phenotypes in PC-3 Tet-on shMAP3K2 cells and cells in which the knockdown is complemented with either wild-type or K260A mutant MAP3K2, which cannot be methylated (Fig. 4F). Here, SMYD3 is linked to posterior cortical atrophy.