It has been scientifically proven that chronic inflammation, typical for asthma, through inflammatory mediators (cytokines) secondarily reduces the CREB (Cyclic adenosine monophosphate Response Element-Binding protein) activity, the level of TRK (Tyrosine Receptors Kinases) protein and release of BDNF (Brain-Derived Neurotrophic Factor) in frontal lobes and the limbic system, which results in damage to the hippocampus and a reduced level of cerebral monoamines [23–25]. The gene discussed is CREB1; the disease is asthma.