Finding. Mitochondria were supposed to sip Fe(II) from the cytosol through mitoferrins. Han, Liu and colleagues watch iron jump the gap at mitochondria-lysosome contacts instead. Structured illumination sees the transfer on those contacts, not in the bulk cytosol. PPS39 and TOMM22 hold the junction. Sideroflexin 1 is the mover. Knock SFXN1 down and mitochondrial Fe(II) falls, even when you set aside SFXN1's serine-transport job. MFRN is not required for this path.
Why this paper matters Iron-loading neurodegeneration and cardiomyopathy papers treat lysosomes as a warehouse and mitoferrin as the only door. A contact-site hose changes chelator logic, MFRN-knockout interpretations, and where you put SFXN1 in disease maps.
Score 92. Canonical rewrite, live imaging, three-protein machine. High confidence for the imaged path; the 'major route' claim still needs a flux fraction.