A previous study demonstrated that TGFβ promotes apoptosis through suppression of the PI3K/Akt signalling pathway in the bovine mammary epithelial cell line BME-UV1. We compared TGFβ modulation of PI3K/Akt signalling and its downstream role in apoptosis and proliferation in two normal bovine mammary epithelial cell lines MAC-T (myoepithelial and luminal-like profile) and BME-UV1 (luminal-like profile). TGFβ induced apoptosis in BME-UV1 cells, while TGFβ rescued MAC-T cells from serum starvation-induced apoptosis. TGFβ reduced PI3K/Akt activity in MAC-T cells suggesting PI3K/Akt modulation is not involved in the antiapoptotic effect of TGFβ in these cells. In BME-UV1 cells, TGFβ had a biphasic effect on PI3K/Akt activity including an initial rise at 3 hours in phosphorylation of Akt followed by a reduction between 12-24 hours. This led us to investigate the effect of Akt inhibition in TGFβ-induced apoptosis of BME-UV1 cells using the Akt inhibitor MK. Enhanced apoptosis of the TGFβ + / MK + group compared to the TGFβ - /MK - control group suggests that Akt inhibition in combination with TGFβ treatment promotes apoptosis of BME-UV1 cells. TGFβ had contrasting effects on apoptosis but not growth arrest, as TGFβ treatment reduced proliferation of both cell lines, and therefore the use of these cell lines as models to study TGFβ signalling should be carefully tailored to the questions asked.