Nicotine is biologically active. It competes with acetylcholine for binding to specific membrane receptors, so-called nicotinic cholinergic receptors (nAChRs). They are widely expressed in the nervous system and skeletal muscle. Nicotinic receptors are also present in many cell types, e.g. epithelial, blood, and cancer cells. When nicotine binds to the nAChRs, the conformation of the receptor subunits changes, opening the receptor channel gate. This allows the influx of sodium and calcium ions into the cell, leading to membrane depolarization. It results in the activation of influx of calcium ions. These processes trigger a cascade of signal-dependent calcium ions. A very significant role of nicotinic receptor in the regulation of apoptosis, angiogenesis as well as in cell division and migration has been recently shown. Nicotine induces growth factors, such as BDNF, VEGF, TGF-a, HGF, VEGF-C, TGF-b, PDGF and has a mitogenic effect on cancer cells. A key role in these processes is played by a serine-threonine kinase Raf and extracellular signal-regulated kinases ERK1-ERK2. Nicotine causes an increase in survival of cancer cells through phosphorylation of serine/threonine protein kinase Akt, which interacts with other proteins, and leads to blockage of apoptosis. Recently it has been shown that nicotine interferes with hormonal signaling. Under the influence of nicotine, the levels of serotonin, dopamine, gamma-aminobutyric acid (GABA), and epinephrine are significantly changed.