Our finding of reduced HSC activation and type I collagen production in a tumor-free model of liver injury induced in iLID3W mice by CCl4 suggests that the reduction in HSC activation in mice with a sustained IGF-I depletion was the consequence rather than the cause of reduced metastasis, indicating that the IGF axis is involved in the wounding response of the liver, independently of the trigger. Here, IGF1 is linked to neoplasm.