The oxidative stress observed in TBE is responsible for the oxidative modifications of cellular components and body fluids, including proteins, lipids and nucleic acids [4, 6], which also favors the modification of the environment of the NFκB transcription factor leading to complex metabolic disorders resulting in pathophysiological changes, including inflammation and exacerbation of the disease process [7]. This evidence concerns the gene NFKB1 and tick-borne encephalitis.