Since R‐Smads are directly phosphorylated by upstream receptor kinases, which then form heteromeric complexes with Smad4 to translocate into the nucleus,37 the zinc deficiency induced by SLC39A5 depletion may barely maintain the Smad protein in a favourable structure for phosphorylation, and may lead to nucleus translocation retention, further impairing the TGF‐β signalling. This evidence concerns the gene SMAD4 and Zinc deficiency.