The advance in systemic treatment of non-small-cell lung carcinoma is so called targeted treatment, as the conventional chemotherapy probably has already exploited all its possibilities in the effectiveness of the treatment. The targeted therapy of lung carcinoma is a selective influencing of intracellular cell signal pathways by acting on various parts of exprimated cell receptors which play a role in proliferation of a malignant cell. “Small molecules” (genefit, erlotinib) cause the inhibition of tyrosine kinase activity of an intracellular part of the EGF (epidermal growth factor) receptor and so they block the signal pathway of protooncogen k-ras leading to proliferation of a malignant cell. The gefitinib effectiveness in the therapy of non-small-cell lung carcinoma is related to EGF receptor mutation in axon 18 - 21; effectiveness of erlotinib is vice versa related to the expression of EGF receptor. Cetuximab acts on intracellular part of the receptor for EGF and it blocks the effective EGF bond and the receptor activation. Angiogenesis inhibition represents the important moment of the tumour nourishment restriction and by that also of the tumour growth. The target of proliferation inhibition of vessel structures is VEGF (vascular endothelial growth factor) and VEGFR (receptor for vascular endothelial factor). VEGFR-2 can be influenced by crowding out or inhibition of VEGF bevacizumab or extra or intracellular receptor domain itself.