Molecular mechanisms of the antiproliferative effect of vitamin K3 (sodium 2,3-dihydro-2-methyl-1,4-naphthoquinone-2-sulfonate) were studied on a human T-lymphoma model (Jurkat cell line). It is shown that a short-term treatment of the cells with vitamin K3 damages their genomic DNA. Further culturing of the cells in the presence of vitamin K3 decreases the expression of the c-myc gene, inhibits the activity of DNA-dependent DNA-polymerases, and leads to the subsequent development of apoptosis. Combined exposure to vitamin K3 and azidothymidine has a synergistic antiproliferative effect.