Plants rely on iron (Fe) for a wealth of biochemical reactions including photosynthesis, respiration and reactive oxygen detoxification. They use two main strategies to mobilize Fe from the soil. Strategy I relies on reduction of FeIII by a membrane ferric chelate reductase and the secretion of coumarins to mobilize soil Fe, making it available for uptake by the divalent metal transporter IRT1. Strategy II, which is used only by graminaceous species, relies on the secretion of phytosiderophores. At some stages, intracellular stores play a critical role in Fe supply. In a plant cell, Fe may be stored in vacuoles or in plastids. We have shown that AtNRAMP3 and 4 are required for Fe mobilisation from embryo vacuoles during germination (Lanquar et al., 2005, EMBO J., 24, 4041-4051). When germinated under Fe deficiency, nramp3nramp4 mutants are strongly chlorotic and their development is arrested. To identify new players in intracellular Fe homeostasis, we have looked for mutations that suppress nramp3nramp4 chlorotic phenotype. In one of the suppressors, the causal mutation affected VIT1, the gene encoding the transporter for Fe uptake into the vacuole (Mary et al., 2015, Plant Physiol. 169(1):748-59). In another one, a mutation in the gene encoding the Pleckstrin Homology protein 1 shifted the localization of AtNRAMP1 from the Trans Golgi Network to the vacuolar membrane where it could compensate for the lack of AtNRAMP3 and 4 (Agorio et al., 2017, PNAS, 114(16):E3354-E3363).