In the future, we will also use a more suitable RIPF evaluating model by using C57BL/6 mice to better evaluate the capacity of IR‐TAM@Alb in depressing RIPF, as well as using some other fibrosis models like hepatic fibrosis, pulmonary fibrosis, renal fibrosis, and et al., to evaluate the extensive feasibility of using IR‐TAM@Alb to depress different fibrosis diseases.[29] All in all, in this well‐designed research, we designed a tumor/fibrosis dual‐targeting and co‐therapy strategy to eradicate RT‐resistant tumors while sparing normal lung tissues. This evidence concerns the gene ALB and pulmonary fibrosis.