One virus family with oncogenic members that could be causative for the development of tumors is the polyomavirus (PyV) family. The number of known human PyV species has increased rapidly, from two species (JCPyV and BKPyV) detected in 1971, to 13-14 species reported since 2007. Most of these viruses were isolated from nasal samples, skin, serum, or stool samples. Despite their recent discovery, many human PyVs are common in the population, and several, including MCPyV, and human PyV 6 and 7 are frequently found in the skin [6]. Polyomavirus are also analyzed in association with some cancers: Merkel cell polyomavirus (MCV) was first identified in Merkel cell carcinoma, and the primary site of productive BK polyomavirus replication is the kidney [6]. The involvement of oncogenic viruses in HNSCC and skin cancers has been evaluated by many authors. A research team from Turku, Finland, detected by qPCR viral DNA of SV40, JCV and BKV from HNSCC samples. The JCV was detected in the highest proportion (37%), proving that JCV could be a cofactor for HNSCC [7]. [PERSON] et al. tested salivary gland tumors and detected a high prevalence of beta human papillomavirus DNA in malignant tumors. In contrast, polyomavirus DNA was present in all categories of tested samples: cancerous and non-cancerous tissues samples. These viruses are thought to be involved in the carcinogenesis of these tumors, which could eventually be proven by further mechanistic studies [8]. By comparison, a research team from Stockholm did not find any association between salivary gland tumors and neither HPVs, nor polyomaviruses [9; 10]. Regarding Herpesviruses' involvement in HNSCC, many studies are referring to EBV and its association with nasopharyngeal cancers, and even more so, some authors are analyzing the possibility of developing a screening test for people at risk, which would detect EBV in liquid biopsies [11]. As for HPV involvement in HNSCC, the scientific literature is abundant, and the prevalence is different for each continent, and is associated with known risk factors (smoking, alcohol). [PERSON] et al. observed a considerable difference regarding HPV prevalence in HNSCC globally, with a general tendency of increasing HPV+ oropharyngeal cancers [12]. [PERSON] et al. detected polyomaviruses in skin cancers, but the authors recognized the necessity of another carcinogenic marker to support the etiologic role of the viruses [13]. [PERSON] et al. analyzed the association between ultraviolet radiation (UVR) and cutaneous viral infections: beta HPV types and polyomaviruses. This association seems to favor skin cancer development [14]. The above-mentioned literature, published by known researchers in the field, presents the possible association between these oncogenic viruses and the HNSCC and skin cancers. We have also tested, so far, different tumor samples for oncogenic viruses, e.g., HPV only [9; 15; 16], for polyomaviruses only [10], for HBV only [17], but we have never tested, until now, tumor samples for viruses belonging to the three different viral families simultaneously. The results of this study will help to understand the mechanism of these cancers, and if the viral etiology could be confirmed, at least as a co-factor. As a consequence, our results can contribute to the development of new therapeutic strategies. A tumor induced by a virus could be efficiently prevented by vaccination or treated by oncolytic viral therapy and/or by targeted therapy, in parallel with preventive measures for other co-factors. Aim: to evaluate the association between DNA of oncogenic viruses from _Papillomavirusae, Herpesviridae_, and _Polyomavirusidae_ families in different HNSCC and skin cancers from Romanian patients, using a sensitive molecular assay.