While being a safe over the counter drug, paracetamol has also proved to be a cytotoxic agent for cultured hepatocellular carcinoma cells (HepG2). In order to understand the biochemical mechanisms underlying its cytotoxic ability, molecular docking of paracetamol with cyclin dependent kinase 2 protein (CDK2) and breast cancer type 2 susceptibility protein (BRCA2) plus cyclooxygenase 1 (COX1) enzyme protein was undergone. Computational simulation was performed using Schrödinger software to describe the details of binding between atoms of the active sites and paracetamol. All COX1, CDK2 and BRCA2 proteins showed binding scores with paracetamol. Their G-scores were -5.32, -5.61 and -6.08 respectively leading to selective inhibition of these proteins and loss of their cell cycle related activity. The binding strength of COX1 and CDK2 with paracetamol was mainly dependent on the hydrophobic residues, while that of BRCA2 was contributed to charged residues. Binding is responsible for the subsequent loss of activity of these cell cycle related proteins and eventual cancer cell death via apoptosis.