PPARA and Keratoconjunctivitis sicca: The greatest differences are seen in neutrophils, myeloid (macrophage and monocyte) and cDC2 cells and include IL-6, LPS-stimulated MAPK, NFkB, IL-17, and PPARα/RXRα signaling pathways that contain mediators relevant to dry eye pathogenesis (8, 37–42).