Pharmacotherapy of psoriasis vulgaris and arthritis includes using anti-cytokine or conventional drugs Unfortunately, during this treatment, the drug-resistance phenomenon was observed and the search for a new class of molecular markers is mandatory. The aim of this study was to evaluate changes in the expression profile of TNF-α and its receptor – TNFR1 and TNFR2 in psoriatic patients during adalimumab, etanercept, ustekinumab or cyclosporine A therapy and clinical scales of treatment effectiveness – PASI, BSA, DAS28, DLQI. The study group consisted of whole blood and serum from psoriatic patients during adalimumab, etanercept, ustekinumab or cyclosporine A pharmacotherapy. Each of these subgroups consisted of 30 patients. Follow-ups were made after 4 years. RTqPCR and MALDI-TOF spectrometry were used. PASI, BSA, DAS28, and DLQI scales were evaluated in each group. HaCaT were exposed to 1µg/ml LPS)in order to induce inflammation and next were treated with adalimumab (8µg/ml) or cyclosporine A (100 ng/ml) for 2, 24 and 48 hours in comparison to untreated cells. To determine the expression of analyzed genes in different microarrays, the ELISA and Western blot tests were performed. The analysis showed that all used drugs changed the expression profile of selected genes at the mRNA and protein level. It An in vitro study confirmed the assessment that drugs act via TNF-α signal paths. Regardless of the drug, the highest differences in the expression of these genes was observed after 2 hours compared to a control. TNF-α and its receptors seem to be useful molecular markers of psoriasis therapy effectiveness.