Similarly, IMs undergo activation and loss during infection and are replenished primarily through circulating monocytes differentiating into proinflammatory IMs, with CD206+ IMs contributing a smaller proliferative component.[160] Together, orchestrated by both niche‐derived signals and inflammatory context, AMs and IMs employ distinct but complementary proliferative strategies to sustain lung immune homeostasis and repair. This evidence concerns the gene MRC1 and infection.