Dysfunction of one or more components of the LFU 1) hinders the composition of tears, and thus its ability to protect the surface epithelium; 2) disrupts the innate and adaptive immune and inflammatory pathways that protect the ocular surface from external stimuli (i.e., exposure, infection); and 3) stimulate the production of proinflammatory cytokines [i.e., interferon (IFN)-γ, interleukin (IL)-1, −6, −8, tumor necrosis factor (TNF)-α, intercellular adhesion molecule (ICAM)-1, among others] by the ocular surface immune and epithelial cells (Roy et al., 2022). The gene discussed is TNF; the disease is infection.