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). This evidence concerns the gene CD79A and Arrhythmogenic right ventricular dysplasia.