Pre-treatment of cells with Akt-specific inhibitor AKTi1/2 did not markedly perturb recruitment of EGFP-SNX18 to the site of bacteria invasion, while the phosphorylation of Akt elicited by wild type S. Typhimurium (but less by ΔsopB mutant) at 10 min post infection was completely abolished (data not shown). The gene discussed is AKT1; the disease is infection.