The midbody is involved in the regulation of cytokinesis and is inherited by one of the daughter cells after cell division. The midbody was thought to be degraded soon after by macroautophagy or released into the extracellular milieu, but recent data indicate it might have postmitotic functions, and promote stemness and tumorigenicity in cancer cells. However, it is unclear how post-mitotic midbodies are retained in cells. Here (p. 4051), Xiao-Jing Wang, Rytis Prekeris and colleagues investigate in more detail the fate of postmitotic midbodies in HeLa cells and in squamous cell carcinoma (SCC), chosen because they contain cancer stem cells (CSCs). They first show that the LC3-binding protein FYCO1 localises to the postmitotic midbody and mediates the formation of isolation membranes around it, thereby initiating autophagy. Interestingly, FYCO1 specifically regulates the autophagy of large cytosolic structures such as the midbody, without affecting the general autophagy flux. To address the role of midbody accumulation in SCCs, the authors isolated the CSC population and found that these cells accumulated more midbodies than other SCC cells. Depletion of FYCO1 in CSCs did not result in an expansion of the stem cell population or its clonogenicity, but significantly increased their ability to form invadopodia in spheroids. This suggests that midbody accumulation, through downregulation of FYCO1, can modulate cancer invasiveness, and further work will address the regulation of this mechanism.