Imagine that you could microinject cytochrome c into the cytosol of both wild-type cells and cells that were lacking both Bax and Bak, which are apoptosis-promoting members of the Bcl-2 family of proteins. Would you expect one, both, or neither of the cell lines to undergo apoptosis?

In the given case, if the cytochrome c was administered within the cytosol of both the cells that were defective doubly for Bax and Bak and the wild type cells then the cell lines would go through the process of apoptosis. Both the Bax and Bak refer to the proteins that come under the Bcl-2 family and plays an essential role in triggering the process of apoptosis.

The cytochrome c administered in the process combines with an adapter protein that further stimulates a procaspase. Thus, due to the combination, the beginning of the caspase cascade takes place, which eventually results in apoptosis.

Though the cells that were devoid of both Bax and Bak fails to discharge cytochrome c from the mitochondria even after attaining the upstream signals, however, due to no issue in the pathway's downstream section because of the stimulation done by the cytosolic cytochrome c, the microinjection of cytochrome c nulls the effect of the doubly defective cells, and starts the process of apoptosis.