Iron acquisition is essential for Mycobacterium tuberculosis (Mtb) virulence. Understanding the molecular mechanisms used by Mtb to scavenge iron during infection might reveal new targets for antimicrobial development. Rv2895c, a homolog of ViuB from Vibrio cholerae has been postulated to be involved in iron-siderophore uptake and utilization in Mtb. This study examines the requirement of Rv2895c for adaptation of Mtb to iron limitation. We show that Rv2895c is dispensable for normal replication of Mtb in iron deficient conditions and in human macrophages. Thus, contrary to the predictions of sequence analysis and in-vitro studies the genetic evidence indicates that in normal conditions Rv2895c is not required for iron acquisition in Mtb.