Replacement of a diseased organ with tissue derived from the same patient is an ideal therapy. However, it is difficult to recreate many adult human tissues in vitro due to the functionally necessary architecture of most organs and the lack of understanding of methods to direct the development of the organ of interest. The parathyroid gland is ideal for in vitro organ development because the parathyroids are an uncomplicated organ system that is affected by a surgical complication rather than a physiological or autoimmune disease. Using undifferentiated hESC lines BGO1 and H1, we successfully promoted expression of pharyngeal endoderm markers by culturing with Activin A and Sonic hedgehog (Shh) and by optimizing the culture protocol serially for the expression of signaling factors in the parathyroid development pathway. Cells that underwent the differentiation protocol expressed and released PTH. Two main barriers exist to using hESC for further studies: (1) the potential of these cells and their progeny for alloimmunity and (2) the potential of the cells to form tumors. Isolating human progenitor cells from the patient that can then be induced to function as parathyroid is preferred. Therefore, we needed to identify a source of autologous progenitor cells that can be used. In humans, the parathyroid glands develop in the third and fourth pharyngeal pouches in contiguity with the developing thymus (third pharyngeal pouch) and parafollicular cells of the thyroid (fourth pharyngeal pouch). Some cells in the thymus express parathyroid markers, but no prior research has been performed to investigate the possible differentiation of thymus into parathyroid cells; although, clinical experience shows that they are not able to do this in situ in spite of physiologic stimulus due to hypoparathyroidism. Thus, we have investigated thymus as a source of autologous endoderm and parathyroid-like precursor cells. Here we show that human thymus cells subjected to our differentiation protocol are induced to express the parathyroid markers PTH, CaSR, CXCR4, and GCM2. The redifferentiated cells release PTH in response to calcium concentration and can be captured using anti-CaSR antibody-coated beads. Our protocol uses a patient’s own tissue, recreates a physiologically controlled system (calcium-regulated PTH release), and does not require genetic manipulation of cells. Thus, our data suggests that it will be possible to restore a patient’s parathyroid function using in vitro redifferentiated cells.