To analyze the safety of UV-A irradiated milk we used western blotting which evaluated the possibility of inducing carcinogenicity on the human cell lines. In our previous published study, at 838 mJ/cm 2 more than 60% reduction of AFB1 and AFM1 was obtained without any significant cytotoxicity on HepG2 cell lines . To further understand the cellular mechanisms and cell apoptosis, we irradiated WM spiked with 3µg/ml of AFs (AFB1 and AFM1 separately) and irradiated under UV-A at doses 279 and 838 mJ/cm 2 . These high concentrations were carefully chosen to see a cellular response. The response of UV-A irradiation on cell stress and apoptosis was investigated by monitoring p53 expression. In cancer development, the p53 gene is the most commonly altered. It acts as a sensor for chromosomal integrity and is triggered by cellular stresses such as hypoxia, and, most critically, DNA damage. Its effects are connected with cell cycle slowdown, allowing time for oxidative stress response, or with induced apoptosis thus preventing injured cells from cell proliferation . The western blot data (Fig. ) showed the reduced phosphorylation of BAD protein in UV-A treated milk samples containing AFB1 toxin. The highest dose of 838 mJ/cm 2 showed a significant difference in the reduction of phosphorylation of BAD (p<0.05). However, p53 expression showed an increase in expression in samples containing AFB1 irrespective of UV-A treatment. Although this increase in p53 expression was not statistically significant. In the case of AFM1, both p-BAD and p53 expression were lower in AFM1 treated samples irrespective of UV treatment. Interestingly, these differences were not statistically significant. More experimental analysis is warranted to validate the outcome of this study.