Table 1.

Murine models associated with obesity and HCC

Gene	KO Phenotype	Advantages and Shortcomings
IL-6	Mature onset of obesity and insulin resistance on HFD; reduced obesity-induced HCC promotion	Advantages: Specific interested gene knockout. Liver tumor formation spontaneously or with environmental treatment. providing direct insight into the physiological roles of genes interested. novel or unexpected actions of target genes may emerge Studying specific gene function in hepatocarcinogenesis Useful in discovering therapeutic targets.
TNFR1	Rapid weight-gain like WT on HFD; ablation of obesity-enhanced HCC development; reduced obesity-induced steatohepatitis	Shortcomings: Disable to fully resemble the pathological characteristics observed in human. Unexpected actions of target genes. Unpredictable further gene mutations in human genome Unknown response to anti-tumor agents
IKKβ	Improved insulin sensitivity; Enhanced DEN-induced HCC development, but protection from LT-induced HCC suggesting that IKKβ and NF-κB activation promote, rather than inhibit, HCC development.
p38α	Enhanced DEN-induced HCC development
NEMO/IK Kγ	Protected from obesity-induced insulin resistance; development of spontaneous liver damage, hepatosteatosis, fibrosis and eventually HCC
TAK-1	Protected from obesity-induced insulin resistance; development of spontaneous liver damage, hepatosteatosis, fibrosis and eventually HCC.
ATG7	Spontaneously multiple benign hepatocellular adenoma development accompanied by mitochondria dysfunction and genomic instability.
ATG5	Spontaneously multiple benign hepatocellular adenoma development accompanied mitochondrial swelling, p62 accumulation, and oxidative stress and genomic damage responses