Additionally, abnormal redox states may facilitate SAMHD1's nuclear relocalization by promoting oxidative modifications of cytoplasmic SAMHD1, enhancing its DNA‐binding capability.[26, 27] Furthermore, our findings suggest that OGD stress promotes nuclear SAMHD1 translocation in hepatoma cells, aligning with the metabolic stress seen in solid tumors due to cancer cells’ high demand for oxygen and glucose.[28, 29] As HCC progresses, however, nuclear SAMHD1 levels decline, shifting toward the cytoplasm. Here, SAMHD1 is linked to cancer.