Environmental factors are known to influence carcinogenesis. Pollutants, such as heterocyclic amines (HAs) and polycyclic aromatic hydrocarbons (PAHs) are examples of environmentally borne procarcinogens. Procarcinogens are not active carcinogens although, they require bio-activation, via enzymes such as cytochrome P450 (CYP) to transform into the active products. CYP1A1 isoform, regulated by aryl hydrocarbon receptor (AhR) plays a significant role in the bio-activation of PAHs and HAs. AhR has multiple co-activators and co-repressors for AhR that have been identified S remarkably. Silencing mediator for retinoid and thyroid hormone receptors (SMRT) were designated as a major co-repressor for AhR. The present study is examined the effect of SMRT overexpression on the cyp1a1 mRNA levels in murine hepatoma Hepa 1c1c7 cell line. Hepa 1c1c7 cells were maintained in Dulbecco’s Modified Eagle Medium (DMEM) and competent cells have successfully been produced using the calcium chloride method. Cells were transformed using plasmid DNA and Lipofectamine. TCDD (2, 3, 7, 8-tetrachlorodibenzo-p-dioxin) was employed as an inducing agent for CYP1A1. The total cellular RNA was isolated and real-time PCR of Cyp1a1 was conducted. A statistical analysis was conducted by using a one-way analysis of variance followed by the Student-Newman-Keuls test. The results showed that cells transfected with the co-repressor SMRT had lower TCDD-mediated induction of cyp1a1 mRNA without affecting constitutive Cyp1a1 mRNA levels, i.e., SMRT was able to significantly decrease inducible Cyp1a1 mRNA levels in Hepa 1c1c7 cells. The present findings also demonstrated that calcium chloride is a convenient method for routine transformation. Thus, this study opens a new avenue for the management of carcinogenesis involving CYP1A1-inducing carcinogens.