Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains one of the leading causes of death worldwide. TB pathogenesis is shaped by a complex interaction between the pathogen and host immune responses, particularly through mechanisms such as oxidative stress and ferroptosis; a form of regulated necrotic cell death driven by iron-dependent lipid peroxidation. This Review highlights recent insights into how Mtb modulates oxidative stress pathways and thus triggers ferroptosis in host cells. Understanding the interplay between oxidative stress responses and cellular and tissue necrosis opens new avenues for therapeutic interventions of TB by controlling bacterial growth and preventing host tissue damage.