The GSEA found that the high-TILRGS subgroup was enriched in arrhythmogenic right ventricular cardiomyopathy, dilated cardiomyopathy, focal adhesion, hypertrophic cardiomyopathy, and regulation of actin cytoskeleton (Fig. 6c), while the low-TILRGS subgroup was enriched in allograft rejection, antigen handling and presentation, the intestinal immune network for IgA production, olfactory transduction, and primary immunodeficiency (Fig. 6d). The gene discussed is CD79A; the disease is arrhythmogenic right ventricular cardiomyopathy.