One possible scenario for our findings would be that upon HCC initiation, the decrease in TLR4-related DNA repair proteins, such as Ku70, and the diminished activity of the so-called senescence response to defense against tumorigenesis in the liver could lead to stimulation of cancerous cell proliferation, attenuation of autophagy and programmed cell death, and promotion of malignant transformation, thus leading to a more aggressive HCC phenotype [16,58,60]. This evidence concerns the gene PROS1 and hepatocellular carcinoma.