More interestingly, in vivo perturbations in EHMT1/GLP and EHMT2/G9a have been implicated in many cellular processes including autophagy [43], DNA methylation, [35, 44], hypoxia [45], tumor suppression [46–49], chromatin remodeling [20], and synaptic plasticity [50] to name a few, and homozygous loss of EHMT1/GLP results in embryonic lethality in mice [51]. The gene discussed is EHMT2; the disease is neoplasm.