Pseudomonas aeruginosa is a gram-negative opportunistic pathogen that can cause life-threatening nosocomial infections in immunocompromised patients. P. aeruginosa requires iron for survival and infection and has evolved several mechanisms to sense and acquire iron from the host including the utilization of heme. PhuS is a cytoplasmic heme binding protein that regulates extracellular heme flux into P. aeruginosa through its conformational flexibility enabling it to exist in functionally distinct forms. The data presented indicates fluctuations in extracellular heme flux through PhuS can disrupt iron homeostasis through the altered expression of the prrF1/prrH sRNA network.