The greatest fold‐change affected Smyd2, which encodes a lysine methyl transferase that suppresses p53 trans‐activation by monomethylation (at residue K370 in human p53).36SMYD2 has been implicated as a target for copy number gain and overexpression in numerous cancer types37 and has been shown to be required for MLL‐AF9 leukemia mouse models where RUNX functions have also been implicated.38, 39 Moreover, interest in SMYD2 as a potential oncogenic driver has led to the identification of several small molecule inhibitors,40, 41, 42 making this an attractive target for further investigation. The gene discussed is SMYD2; the disease is leukemia.