Furthermore, we have shown how integrating the DMR results provided by ABBA with other “omics” data (RNA-seq and ChIP-seq generated in the same experimental system), enabled us to generate new hypotheses for the mechanism underpinning the disease, revealing a candidate gene (Ifitm3) for the susceptibility to glomerulonephritis. This evidence concerns the gene IFITM3 and glomerulonephritis.