Comparative analysis revealed that Tu-Gr1+CD11b+–primed 4T1 cells expressed both SCA1-positive and SCA1-negative signatures (Figure 3C), suggesting that Tu-Gr1+CD11b+ may twist tumor plasticity by converting the 4T1-SCA1– cells into 4T1-SCA1+ cells, rather than expanding the preexisting 4T1-SCA1+ population. The gene discussed is ITGAM; the disease is neoplasm.