As shown, targeted therapies without or poor monoactivity can provide important impact on clinical outcome following tumor tissue editing, e.g. the addition of mammalian target of rapamycin (mTOR) inhibitors, azacitidine, α-interferon, cell cycle-dependent protein kinases four and six (CDK4/6) inhibitors, elotuzmumab etc. (9, 21, 22, 25–27).This separation in two steps is to some extent arbitrary, as both therapeutic steps are interwoven and strengthen one another as revealed by data on clinical trials (Figure 1). This evidence concerns the gene MTOR and neoplasm.