WHO grade II–IV gliomas are profiled for a number of genes such as MGMT, TP53 and IDH1/2 or their proteins or other proteins such as KI-67 [1]. The combined profile of an individual glioma is of prognostic value and guides therapeutic choices in neuro-oncology group meetings—which is totally amazing as the present profiling only scratches the surface of the enormous bioinformatic data within the entire tissue volume of the profiled glioma. It is easier to believe that a gene here or a protein there does not mean much. Philately of studying a single gene or protein expression in gliomas is mostly (1) outdated in the era of genomics and any omics and (2) fails to suggest new targets for synthetic antitumor drugs, which are thousands in store but will never be tested in gliomas with the present validation method of randomized multicenter trials. Or the reader should at least be provided with analyses and figures of the signaling pathways involved. By DNA and RNA sequencing, we have just surveyed the ground floor of the department store of genomic information in each of our cells—and we know little of the information available in the upper floors (methylome, acetylome, histonome, etc.) up to the chromosomes (‘chromosome’?). No one with a recent medical education can think that our body and brain are made from some 20,000 genes in our cells, making only some 1 % of the whole genome. How is it possible that a fly with a pitiful 100.000 to 250.00 neurons can fly so precisely and quickly? This is because those neurons make a formidable aerobatic network of some 10 synapses. Our own brain—the most complex machine in the known universe—contains some 10 synapses, an unimaginable network exceeding the combined capacity of all the computers in the world! This leads to three obvious questions: