Psoriasis is a benign, chronic skin disease characterized by keratinocyte hyperproliferation and abnormal differentiation. Telomerase is an enzyme-reverse transcriptase that protects chromosomes from degradation by stabilizing telomere length. Recent studies suggest that telomerase activity (TA) may be responsible in part for some of nonmalignant proliferative skin diseases. There is evidence that telomerase has an active anti-apoptotic role. TA in general is associated with cellular proliferation. We hypothesize a relationship between TA, keratinocyte proliferation and apoptosis in psoriatic skin lesions. The TA in telomere elongation makes keratinocyte hyperproliferation possible and is at the same time, one of its limiting factors. This hyperproliferation in psoriasis occurs as a result of significant keratinocyte damage caused by self-reactive T-cells through induction of various apoptotic pathways. On the other hand, TA in telomere elongation, together with other factors, has an active anti-apoptotic role, preserving the necessary amount of equilibrium between these two processes (apoptosis and proliferation) therefore being the main reason why conversion of a psoriatic plaque to squamous cell carcinoma is rare. As there is little data on TA in psoriatic lesions, in evaluation of our hypothesis we suggest thorough parallel studies of TA, telomere length, apoptosis and proliferation in psoriatic lesional skin on multiple checkpoints and targets, using more samples so the reliability of the results would be higher. This is important since a better understanding of these factors might provide new possible therapeutic targets.