A range of histone and non-histone proteinsubstrates are lysine N-methylated by methyl transfer from the SAM(S-adenosyl-l-methionine) cofactor of SMYD3.Notably, loss of SMYD3 catalytic activity inhibited tumorigenesisin the presence of oncogenic Ras,1 suggestingthat inhibition of SMYD3 in cancers with elevated RAS pathway signalingmay be a useful therapeutic strategy. The gene discussed is SMYD3; the disease is cancer.