As a possible mechanism of action in terms of an anti-oncogenic effect, statins have been reported to inhibit vascular endothelial growth factor receptor (VEGFR) and epidermal growth factor receptor (EGFR) signaling, to enhance the effect of receptor-tyrosine-kinase-inhibitors such as gefitinib and sorafenib [16–21], and to overcome EGFR-tyrosine-kinase-inhibitor resistance in non-small cell lung cancer (NSCLC) cells and thus improve progression free survival of NSCLC patients treated with EGFR-tyrosine-kinase-inhibitors [22, 23]. This evidence concerns the gene NTRK1 and non-small cell lung carcinoma.