We could not compare the prognostic value of PTEN and HPV infection in the present study, because lack of uncensored data in HPV-positive group precluded such analysis. Nevertheless, lack of correlation between PTEN expression and HPV infection indicate that these two variables are independent. The analysis, as shown, refer to our recently published results on the prognostic and predictive value of five molecular markers and the presence of HPV infection. We had proposed a prognostic index for recurrence after postoperative radiotherapy that incorporated three factors of the greatest importance: expression of EGFR, expression of nm23, and invasion of the neck nodes. Several clinical studies demonstrated the potential of molecular profiles to predict the benefit from accelerated radiotherapy, including our previous report on molecular markers in the pCAIR trial. The results of the present study indicate that the expression of PTEN may be useful in predicting the benefit from accelerated radiotherapy: the patients with high PTEN expression have a favourable outcome after accelerated postoperative radiotherapy, compared to the patients treated with conventional fractionation and to those with low PTEN expression. The clinical significance of this finding is limited by current evidence-based prescription practice that would Methicillin sodium salt favour postoperative radiochemotherapy over postoperative radiotherapy alone in high-risk HNSCC. However, the emerging data on molecular markers and HPV infection raise several questions over actual need of chemoradiotherapy in patients who would, likely, have favourable outcome after postoperative radiotherapy alone. We hope that future clinical trials and research on molecular markers will further address this important concern. A possible role of PTEN loss in the pathogenesis of HNSCC has been described by Califano in his stepwise model of carcinogenesis. Later, a whole spectrum of functional and structural dysfunctions of PTEN in HNSCC was demonstrated, including mutations, losses of heterozygocity, and epigenetic silencing. The majority of these disorders lead to a decrease or loss of protein expression, thus giving the rationale for defective PTEN detection by immunohistochemistry. Recently, a new model of PTEN role in Folinic acid calcium salt pentahydrate cancer development has been proposed and verified in vivo. According to this model, subtle reduction in dose of PTEN, altered the biology of cancer and the expression profiles of genes involved in a cancer cell proliferation. Because of the diverse expression of PTEN in normal tissues and individual tumors, as well as the crucial role of subtle variations of PTEN concentration for cancer phenotype development.