The biological mechanism underlying the progression of non-alcoholic fatty liver disease (NAFLD) to hepatocellular carcinoma (HCC) had never been explored in a systematic, unbiased manner using publicly available data from independent transcriptomic studies. Herein, we reconstructed two regulatory networks centered on transcriptional factors and their putative targets and analyzed whether these regulons were enriched for genes that were deregulated across the three different phenotypes – non-alcoholic fatty liver (NAFL) or steatosis, non-alcoholic steatohepatitis (NASH) and HCC – against two reference network backgrounds. One network was normal liver (TN1) and the other one was cirrhotic liver (TN2). We found that only androgen receptor (AR), adipocyte enhancer-binding protein 1 (AEBP1) and Nuclear receptor subfamily 1 group I member 3 (NR1I3) are common master regulators that may constitute a genetic risk for the progression of NAFLD to HCC and that these findings had a high stringency threshold (p-value=0.001) with consensus across both inference networks – TN1 and TN2. Of additional importance, we explored the number of transcriptional targets they affected and how closely they were connected, and predicted their Mode of Action (MoA). We discovered that AR MoA shares large number of common targets with AEBP1 and NR1I3. Other regulatory units such as Nuclear Factor, Erythroid 2 Like 2 (NFE2L2) known to be involved in the progression of chronic liver disease were deregulated (p-value=0.05) only in TN1. NFE2L2 was predicted to be in a repressed state in NALF and HCC. Lastly we compared our previous outcomes using a human expression profile to a recently proposed experimental model, Mus musculus, to study the changes during NASH-associated liver carcinogenesis finding a remarkable similarity. Further experimental validation is needed to determine the potential role of these regulators of genetic risk to understand the progression of NAFLD to HCC.