Blocking the rise in Ca2+ and thus the repair response resulted in far more necrosis. This is presumably a consequence of breaching the plasma membrane barrier. Necrosis is induced before there is time to induce the slower process of apoptosis, which tends to sequester intracellular proteins and thus avoid unwanted autoimmune responses.
If the plasma membrane is being repaired, perforin is probably acting within endosomes to release granzymes into the cytoplasm. The Boston group gathered more evidence for this theory, but they still want to find out how perforin induces higher levels of endocytosis, and what changes within the endosome turn on perforin's pore-forming activity.