Multiple previous studies have confirmed LCD’s ability to improve SLE symptoms in MRL/lpr mice through various mechanisms, including reducing IRAK1 activation and downstream inflammatory signaling (7, 14, 29, 30), while also ameliorating disease progression by inhibiting effector B cell activation and regulating T cell metabolic reprogramming (31, 32), establishing a strong foundation for the current investigation. This evidence concerns the gene IRAK1 and lattice corneal dystrophy type I.