Breast cancer is the most common cancer in women and the second leading cause of death among women. In addition to growth factors and growth factor receptors, accumulating evidence indicates that aberrant activation of G-protein coupled receptors (GPCRs) and G proteins is involved in the initiation, proliferation and metastasis of breast cancers. GPCRs are the largest family of cell receptors that transmit signals through heterotrimeric G proteins composed of α, β and γ subunits. Gβ and Gγ form a dimer and associate with Gα in the inactive state. Activation of G proteins leads to the dissociation of Gα from the Gβγ. Both free Gα and Gβγ can activate diverse downstream effectors ranging from enzymes to ion channels to control many cellular processes. We have shown previously that Gβγ plays a critical role in mediating effects from divergent GPCRs on breast tumor growth and metastasis both in vitro and in vivo (Tang X, et. al., JBC, 2011, …). In this study we evaluate the inhibition of cell growth using different drugs at various concentrations, and analyzing the data to determine the drugs optimal performance. Therefore, the luciferase and MTT assay where utilized as methods to determine the viability of the cancerous cell. Breast cancer cells from the line MDA-MB-231 were culture in a 6 inch dish. A specific amount of cells were prepared in a 96 well plate, in which one of each drug at descending concentrations was added to each column. The drugs used were M119, M119B, M119C, M119H, M119E, M158C, M119K, ZJ and Gallein. A very consistent data was obtain in both the luciferase and MTT assay and was found that in higher concentrations the drug M119H promoted cell survival. Therefore, Gβγ is involved in a mechanism which helps the proliferation and survival of malignant cells, so if we can identified the specific pathway that takes place in this event it can be of help for future treatment of breast cancer. "