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Small-molecule inhibitors have revolutionized the treatment of cancer and autoimmune disease. Inhibitors of the mammalian target of rapamycin (mTOR), Janus kinases (JAK), and B-cell lymphoma-2 (BCL-2) are three of the most successful therapeutics developed. They target intracellular signaling pathways involved in cell survival, proliferation, and metabolism, processes that are frequently dysregulated in autoimmunity and neoplasia. The inhibition of such pathways also affects physiological processes in various tissues, including mucosal linings and immune cells. Thus, the cost of such treatment often entails higher rates of infectious complications, which holds true for mTOR and JAK inhibition. In addition, JAK inhibitors specifically elevate the risk for herpes zoster, while mTOR inhibitors uniquely reduce the frequency of cytomegalovirus infection. The mechanism that links these inhibitors to particular infections is not yet fully elucidated, and a multitude of factors are likely involved. BCL-2 inhibitors were recently approved and have not been directly associated with infectious complications. Due to the paucity of trials aiming to study infectious adverse events, future research may still unveil infections linked to BCL-2 inhibition.

DOI: 10.1007/978-3-031-11363-5_16