Although Li et al. report that activation of KLF4 contributes to macrophage-like VSMC phenotype modulation during atherogenesis (Li et al. 2021a), Alencar et al. suggest that instead of a terminal state of VSMCs switching to macrophages as originally postulated (Shankman et al. 2015), activation of Lgals3, typically considered as a marker for macrophages, appears to be an earlier transitional state during atherosclerosis. The gene discussed is LGALS3; the disease is atherosclerosis.