VDR and rickets: This predominance of cytoplasmic staining may be explained by our use of a C-terminal antibody clone (against amino acids 344–424 of the human VDR), low-pH citrate retrieval that may insufficiently unmask nuclear epitopes for this clone, restriction of the sample set to rASRM stage III–IV lesions, and predominance of hypovitaminosis D cases, all of which favor cytoplasmic retention of unliganded or phosphorylated VDR capable of both genomic shuttling and rapid non-genomic signaling [39,40].