For example, our previous study showed that a CD10+GPR77+ CAF subset enhances tumor progression via IL‐6 and IL‐8, which is initiated by the complement‐GPR77 signal.[25] In contrast, another study reported an IKKβ‐driven subset of CAFs expressing Col1a2, which suppresses intestinal tumor growth.[68] Therefore, we and others have shown that the hurdle of CAF‐oriented therapy can be circumvented by selectively targeting specific tumor‐promoting CAF subsets. The gene discussed is COL1A2; the disease is neoplasm.