In addition to the difficulties in drug design and synthesis, understanding that downregulation of PKC protein and thus decreased PKC activity upon prolonged strong PKC activation is actually responsible for the tumor-promoting effects of ultrapotent PKC agonists has only recently led to the reversal of PKC-related dogma: for the treatment of cancer, PKC activators that do not cause downregulation should be developed instead of inhibitors (Antal et al., 2015; Newton and Brognard, 2017). This evidence concerns the gene PRRT2 and neoplasm.