Fusarium solani is a soil-borne pathogen devastating agricultural crops throughout the world. While most pathogens are host specific, the fusaria are able to infect both plants and animals. In 2004, an outbreak of Fusarium occurred in association with contact lens wear. Several species of Fusarium were involved but F. solani and F. oxysporum were most prominent. In this work, we have identified a MAP kinase (MAPK), highly similar to fmk1 in F. oxysporum, belonging to the YERK1 subfamily of extracellular regulated kinases. Directed disruption of fmk1 in F. solani AFR4 (FSSC 1) affected several aspects of fungal growth and pathogenicity. Colonies of AFR4„½fmk1 displayed pigmented colony-like formation as opposed to the cottony-white diffuse growth observed with the wild-type strain. Mutants displayed changes in morphology and conidiation patterns with AFR4„½fmk1 mutants producing increased amounts of macroconidia vs. microconidia. AFR4„½fmk1 germ tube emergence was similar to that of wild-type AFR4 and wet weight growth was equivalent but germinules were not able to sense nutrient in chemotropic assays. The disruption of fmk1 increased spore surface hydrophobicity leading to a decrease in association with commercially available hydrogel contact lenses. FMK1 did not affect unworn lens penetration in phosphate buffered saline as both wild-type and mutant strains were able to penetrate commercially available silicone hydrogel contact lenses. AFR4 displayed increased penetration of silicone lenses and this is likely due to: increased spore/lens association, and the inability of AFR4„½fmk1 macroconidia to germinate in phosphate buffered saline. Diminished invasive growth was also noted with disruption of fmk1. Wild-type AFR4 was detected throughout the eye after conidial microinjection while AFR4„½fmk1 was limited to the vitreous fluid. The reduced invasive growth seen is attributed to the loss of chemotropism. The ability to sense and respond to the environment is essential for pathogenicity. MAPK has been deemed essential for plant pathogenicity and now, with its affect on chemotropism, appears to be necessary for animal pathogenicity. FMK1 plays a conserved role in the pathogenicity of Fusarium.