The main obejctive of the project was to evaluate the genetic stability of hiPSC- derived chondrocytes treated with ionizing radiation (IR). The investigations are focused on so far little-known DNA damage response (DDR) in stem-derived cells. In the experiment three types of cell lines were used: hiPSCs reprogrammed from primary human dermal fibroblasts, human articular chondrocytes (HC-402-05a, ATCC) and chondrocyte-like cells differentiated via emryoid bodies from hiPSCs. The investigated cells were treated with IR (0; 1; 2; 5 Gy) and collected 1, 5, 9 and 24 h after IR. The analyses of double strand breaks (DSBs) formation (γH2AX staining), and level of apoptosis (cPARP) by flow cytometry were performed. We also investigated the level of senescence in cells treated with IR (colorimetric assay). Finally, we assessed the changes in chondrogenic markers: CD44, CD151, CD105 and CD49c in hiPSCs-derived chondrocytes treated with IR by flow cytometry. Kinetics of DSBs significantly differ in hiPSCs, chondrocytes, and chondrocyte-like cells differentiated from hiPSCs. Nevertheless, the formation of DSBs in hiPSC-derived chondrocytes is similar to processes occurring in hiPSCs rather than in human articular chondrocytes. The hiPSCs and hiPSC-derived chondrocytes are very prone to DNA damage in comparison with fully mature chondrocytes. It is important to point out that hiPSC-derived chondrocytes possess more efficient DNA repair mechanisms resulting in the lower level of DSBs after 24h, in contrast to hiPSCs. Consequently, hiPSC-derived chondrocytes did not easily undergo apoptosis as hiPSCs. Nevertheless, the hiPSC-derived chondrocytes also reveal increased level of cells undergoing senescence. We aso found that hiPSC-derived chondrocytes do not lose their chondrogenic potential 24h after IR. We demonstrated that induced DDR mechanisms of stem-derived cells remarkably differ from those in “parental” SCs and mature adult chondrocytes. The obtained results contribute to the establishment of reliable, effective and first of all safe hiPSC- based approach for clinical cartilage repair and treatment.