In multicellular organisms, tissue integrity and organ size are maintained through removal of aberrant or damaged cells and compensatory proliferation. The sensing and removal of aberrant cells by their neighbors involve cell competition, a remarkable homeostatic process at the cellular level. In proliferating tissues, cell division is the primary strategy winner cells use to compensate for the loss of loser cells during cell competition. In post-mitotic Drosophila follicular epithelia, however, we have shown that the loss of local tissue volume resulting from loser-cells elimination triggers sporadic cellular hypertrophy to repair the tissue. This ‘‘compensatory cellular hypertrophy’’ (CCH) is implemented by polyploidization through the endocycle, a variant cell cycle composed of DNA synthesis and gap phases without mitosis, dependent on activation of the insulin/IGF-like signaling (IIS) pathway. Furthermore, several lines of evidence in our study suggest that the IIS-dependent CCH is triggered by tensile forces resulting from the elimination of loser cells. Using stretched follicle cells as a model system, we found that a transient receptor potential (TRP) channel is involved in the process of mechanotransduction. Given the fact that similar hypertrophic cellular growth can be observed in different contexts such as Drosophila epidermis, mammalian hepatocytes or corneal endothelial cells, the tension-induced compensatory cellular hypertrophy is likely a conserved strategy for postmitotic tissue homeostasis.