Breast cancer is a global health concern and is a major cause of death among women. In Oman, it is themost common cancer in women, with an incidence rate of 15.6 per 100,000 Omani females. Various anticancerremedies have been discovered from natural products in the past and the search is continuing for additionalexamples. Cytotoxic natural compounds may have a major role in cancer therapy either in potentiating theeffect of chemotherapy or reducing its harmful effects. Recently, a few studies have reported advantages of usingcrude camel milk in treating some forms of cancer. However, no adequate data are available on the lyophilisedcamel’s milk responsibility for triggering apoptosis and oxidative stress associated with human breast cancer.The present study aimed to address the role of the lyophilised camel’s milk in inducing proliferation repressionof BT-474 and HEp-2 cells compared with the non-cancer HCC1937 BL cell line. Lyophilized camel’s milkfundamentally repressed BT-474 cells growth and proliferation through the initiation of either the intrinsic andextrinsic apoptotic pathways as indicated by both caspase-3 mRNA and its action level, and induction of deathreceptors in BT-474 but not the HEp-2 cell line. In addition, lyophilised camel’s milk enhanced the expressionof oxidative stress markers, heme-oxygenase-1 and reactive oxygen species production in BT-474 cells. Increasein caspase-3 mRNA levels by the lyophilised camel’s milk was completely prevented by the actinomycin D,a transcriptional inhibitor. This suggests that lyophilized camel’s milk increased newly synthesized RNA.Interestingly,it significantly (p<0.003) repressed the growth of HEp-2 cells and BT-474 cells after treatment for72 hours while 24 hours treatment repressed BT-474 cells alone. This finding suggests that the lyophilised camel’smilk might instigate apoptosis through initiation of an alternative apoptotic pathway.