For example, hepatic dysfunction in fatty liver disease may promote hepatocellular carcinoma through chronic inflammation and compensatory hepatocyte proliferation; insulin resistance may drive endometrial cancer via hormonal imbalances that favor estrogen signaling; metabolic dysfunction may promote colorectal cancer by enhancing insulin/IGF-1 activity and epithelial proliferation; systemic inflammation associated with metabolic disease may foster a pro-tumorigenic environment in the pancreas; and respiratory dysfunction may exacerbate hypoxia and oxidative stress in lung tissue. This evidence concerns the gene IGF1 and hepatocellular carcinoma.