One can envision a clinical trial architecture in which induction with cancer neuroscience or epigenetic agents, those which target tumor–neuron interactions, such as glutamatergic signaling inhibitors or neuronal activity-modifying drugs, “prepare” tumor and TME, as evidenced by enhanced MHC presentation and immune cell infiltration, followed by optimally delivered cellular immunotherapies (Table 4) [78, 86]. The gene discussed is HLA-C; the disease is neoplasm.