Varicella-zoster virus (VZV) is a highly prevalent pathogen primarily recognized for causing chickenpox during primary infection, and herpes zoster (HZ), also known as shingles, upon reactivation. While post-infectious complications of VZV, such as encephalitis, pneumonia, and post-herpetic neuralgia, are well-established, recent large population-based studies suggest that HZ may increase the risk of occult cancers. This has sparked discussions on the need for cancer screening in patients with HZ to improve early diagnosis and prognosis. However, the specific types of cancers most strongly associated with VZV reactivation have not been systematically identified, and the subsequent cancer risk remains inconclusive. Emerging evidence suggests that VZV may also modulate key oncogenic pathways, such as the inhibition of apoptosis, alteration of cell cycle regulatory enzymes, and interference with immunosurveillance, which could potentially promote cancer development. These findings indicate that VZV’s role in cancer biology extends beyond merely increasing cancer risk and may involve direct cellular manipulation that facilitates oncogenesis. Understanding the interplay between VZV and cancer is critical for public health. Further exploration of the mechanisms of viral oncogenesis could provide valuable insights into how VZV contributes to cancer development and open avenues for targeted preventive and therapeutic strategies.