Tyrosine kinase inhibitors likely cause increased infection risk through a variety of mechanisms, including B cell dysfunction, worsening neutropenia, and, possibly, due to inhibitory effects on IL-2–inducible T cell kinase (in the case of ibrutinib); idelalisib, in particular, appears to be associated with a heightened risk of opportunistic infections including disseminated herpes virus infections and P. jirovecii pneumonia [40, 41]. The gene discussed is IL2; the disease is infection.