FGF-1, one of the most studied members of the fibroblast growth factor family, is a powerful mitogen exhibiting strong action on many different cell types. FGF-1 activity can be mediated not only by autocrine/paracrine pathways but also by an intracrine pathway. FGF-1 lacks a secretion signal peptide and is exported through a non-classical pathway. Endogenous FGF-1 is found in the nucleus of most cell types. Nuclear localization is required for FGF-1 mitogenic activity. FGF-1 promotes tumor development by promoting cancer cell proliferation and survival. Increased FGF-1 expression in early stages of many different cancers has been reported. MCF-7 breast cancer cell line overexpressing FGF-1 can form vascularized, metastatic tumors when injected into ovariectomized or tamoxifen-treated nude mice. FGF-1 also induces angiogenesis in vitro and in vivo. Thus, FGF-1 is an attractive candidate for cancer immunotargeting. FGF-1 is also involved in neuronal cell differentiation and survival. FGF-1 is highly expressed in motor neurons. In response to damage, motor neurons can release FGF-1 which results in astrocyte activation. Under oxidative stress, astrocytes can also release FGF-1 which stimulates ApoE/HDL generation in an autocrine manner for protection of the brain against oxidative stress. Involvement of FGF-1 in inflammation, cardioprotection, wound healing, adipocyte remodeling, and restenosis is also reported.