Cell competition is a form of cell-cell interaction that can eliminate oncogenic mutant cells from the epithelia tissue. For instance, clones of oncogenic cells mutant for apico-basal polarity genes such as scrib or dlg are actively eliminated from the tissue when surrounded by wild-type cells. We have recently identified the Sas-PTP10D system as a ligand-receptor system required for this tumor-suppressive cell competition. To investigate the physiological role of the Sas-PTP10D system, we focused on the process of wound healing, as it is crucial for epithelial homeostasis and has been considered to share a common principle with cancer, namely cancer as an overhealing wound. After cutting the Drosophila wing imaginal disc, the wound is usually healed during development and it generates a normal wing in the adult. We found that defects in the Sas-PTP10D system significantly inhibited the wound healing. Our data also indicated that the Sas-PTP10D system regulates wound healing by modulating the Hippo pathway through EGFR and JNK signaling. The mechanism by which the Sas-PTP10D system regulates wound healing will be discussed.