Recent studies suggest that the plant mitochondrion may play a role during biotic stress responses, such as those occurring during incompatible plant–pathogen interactions. There are indications that signal molecules or pathways initiated by such interactions may directly or indirectly target mitochondrial components and that an important consequence of this targeting is an early disruption of mitochondrial homeostasis, resulting in an increased generation of mitochondrial reactive oxygen species (mROS). These mROS may then initiate further mitochondrial dysfunction and further mROS generation in a self-amplifying manner. The mROS, as well as the graded dysfunction of the mitochondrion may act as cellular signals that initiate graded cellular responses ranging from defense gene induction to initiation of programmed cell death. However, these events may be attenuated by the unique components of the plant electron transport chain that act to substitute for dysfunctional components, dampen mROS generation or facilitate in defining the cellular level of ROS and antioxidant defense systems.