Candida albicans filamentation, the ability to convert from oval yeast cells to elongated hyphal cells, is a key factor in its pathogenesis. Previous work has shown that the integral membrane protein Dfi1 is required for filamentation in cells grown in contact with a semi-solid surface. Investigations into the downstream targets of the Dfi1 pathway revealed potential links to two transcription factors – Sef1 and Czf1. Sef1 regulates iron uptake and iron utilization genes in low iron conditions, leading us to hypothesize that there exists a link between iron availability and contact-dependent invasive filamentation. Here, we showed that Sef1 was not required for contact dependent filamentation, but it was required for WT expression levels of a number of genes during growth in contact conditions. Czf1 is required for contact-dependent filamentation and for WT levels of expression of several genes. Constitutive expression and activation of either Sef1 or Czf1 individually in a dfi1 null strain resulted in a complete rescue of the dfi1 null filamentation defect. Because Sef1 is normally activated in low-iron environments, we embedded WT and dfi1 null cells in iron-free agar medium supplemented with various concentrations of Ferrous Ammonium Sulfate (FAS). dfi1 null cells embedded in media with a low concentration of iron (20uM FAS) showed increased filamentation in comparison to mutant cells embedded in higher concentrations of iron (50-500uM). WT cells produced filamentous colonies in all concentrations. Together, this data indicates that Dfi1, Czf1, Sef1, and environmental iron regulate C. albicans contact-dependent filamentation.