The larvae of the frog Xenopus laevis is capable of regenerating lenses. In this re- generative process, the corneal tissue is capable of forming a lens after removal of the original lens, but the molecular mechanisms for this process is unknown. This dissertation examines the relationship between FGF signaling and lens regeneration, exploring the hypothesis that the FGF signaling plays a key role in triggering lens regeneration. First, the mRNA expression levels of FGFs and FGFRs in the cornea and retina were observed, as the key ligand from the retina travels to the cornea to interact with its receptor and trigger lens regeneration. The described experiments found that FGF1, FGF8, and FGF9 mRNA are more expressed in the retina than the cornea, indicating that they may be the signal for inducing lens regeneration. Three receptor mRNAs (FGFR1, FGFR2, and FGFR3) were found to be expressed in the cornea. Second, the necessity of FGFR signaling was investigated in vitro using a small molecule inhibitor (SU5402) and dominant negative FGFR1. Both experiments demonstrated that lens regeneration is inhibited upon FGFR signaling inhibition, indicating the necessity of FGFR signaling in lens regeneration. Finally, the sufficiency of various factors for lens regeneration was tested using an in vitro cornea culture assay. FGF1 strongly induced lens formation, and FGF8 also appeared to weakly induce lens formation, whereas FGF2 and FGF9 did not induce lens formation. In addition, insulin and FBS also appeared to induce lens formation in cornea cultures. Overall, this dissertation illuminates the roles that FGF signaling play in Xenopus laevis lens regeneration. In the future, this work may guide subsequent research in treating eye diseases.