Overexpression of two hyperpolarizing potassium channels, Kv1.5 and an overactive Kir2.1 mutant,47–49 led to respective significant decreases of 35.3 +/− 17.4 and 39.0 +/− 2.0% in survival after infection (Fig. 1c), confirming at the molecular-genetic level the outcome previously obtained with chemical hyperpolarization. Here, KCNJ2 is linked to infection.