All the above suggests that i) OC methylotype shows specific altered DNA methylation patterns in the course of tumor initiation and progression [59]; ii) the promoter hypermethylation is a leading cause of tumor suppressors’ inhibition in OC pathogenesis [63]; and iii) the loss of function of the high affinity MT1 may be pivotal in the etiopathogenesis of OC. The gene discussed is MTNR1A; the disease is neoplasm.