A three-gene model further showed potential clinical utility (AUC 0.872–1.00 in discovery; 0.665–0.928 in validation).These signatures align with therapeutic axes in SLE (IFN/JAK-STAT) and intersect inflammatory-metabolic pathways in T2DM, supporting assayable biomarkers and compact diagnostic models that warrant validation in larger, medication-annotated cohorts. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.