Given that NK cells in perf−/− mice expressed gzmB at levels similar to those in WT mice, but these mice were severely deficient in rejection of MHC-Ineg targets, the gain of cytotoxic effector function observed after infection-mediated activation of NK cells is likely not due to the observed gain in gzmB protein expression after activation, but more likely due to the concurrent gain in perforin protein expression [8]. Here, PRF1 is linked to infection.