KRAS and infection: The question of differences between smokers and non-smokers seems to play a role not only in oral SCC, but also in lung SCC [17], suggesting that different characteristics like mutations in the p53 and K-ras genes [18], HPV 16/18 infections [19], or outcome after treatment with epidermal growth factor receptor tyrosind kinase (EGFR-TH) inhibitors lead to a unique entity in non-smokers.