In examining the infection dynamics of bacteria internalized after CNF1 treatment, we concluded, based on the inability of CNF1 C866A to promote invasion in the absence of VopC or to increase invasion above untreated levels, that the CNF1-dependent increase in the invasion of HeLa cells by CAB2, CAB2ΔvopC, and CAB4 was attributable to the catalytic activity of the CNF1 (Fig. 3). The gene discussed is CACNB4; the disease is infection.