As shown in Figure 4a, in the absence of bacterial infection or upon infection with the control MC1 ΔcdtB strain, both APC‐proficient and APC‐deficient cells exhibited contact inhibition over the course of the experiment, as assessed by a time‐dependent decrease in the number of Ki67 positive cells and a significant accumulation of cells in the G1 phase of the cell cycle at 72‐hr postinfection (Figure 4b). The gene discussed is ATP7A; the disease is bacterial infectious disease.