  Recent research shows that a faulty or sub-optimally operating metabolic
network can often be rescued by the targeted removal of enzyme-coding
genes--the exact opposite of what traditional gene therapy would suggest.
Predictions go as far as to assert that certain gene knockouts can restore the
growth of otherwise nonviable gene-deficient cells. Many questions follow from
this discovery: What are the underlying mechanisms? How generalizable is this
effect? What are the potential applications? Here, I will approach these
questions from the perspective of compensatory perturbations on networks.
Relations will be drawn between such synthetic rescues and naturally occurring
cascades of reaction inactivation, as well as their analogues in physical and
other biological networks. I will specially discuss how rescue interactions can
lead to the rational design of antagonistic drug combinations that select
against resistance and how they can illuminate medical research on cancer,
antibiotics, and metabolic diseases.
