SREBF2 and complement deficiency: Mapping the differential expression to the DisGenNet disease signature database42 showed that the Normal/NAFLD genes were enriched for signatures of complement deficiency and fatty liver disease, whereas the NASH genes were enriched for neoplastic signatures (Fig. 3G) and analysis of the altered genes for transcription factor drivers showed that genes in the Normal/NAFLD group were driven by metabolism related transcription factors such as C/EBPα/β, ATF6 and SREBP2, whereas genes in the NASH group were driven by inflammatory pathways such as NFκB, and RelA (Fig. 3H).