initiated when epithelial cells form adherens junctions , this is followed by the generation og actomyosin-contractility. The combination of this processes drives cell engulfment by neighbor cell. After internalization, the inner cell is usually killed and digested by the outer cell. This process involves non-canonical autophagy, formation of lysosomes and nutrient recovery. In general, entosis greatly depends on cytoeskeletal structure changes and biophysical forces during the creation of cell-in-cell structures . Novel degradation and signaling pathways are employed during the inner cell killing and digestion process. Entosis in cancer Entosis has been found to be a different mechanism for cancer cells to form cell-in-cell structures at tumor sites. The entosis process in cancer cells is mediated via E-cadherin and P-cadherin. Since cadherins usually create homolytic cell to cell junctions, it is believed that the process mainly occurs between homologous cells. After cell-cell adhesions are mediated, the engulfed cells promote their own uptake into the neighbor cell. Additionally, they promote the ingestion process through actin polymerization and myosin contraction. The invading cell (outer cell) actomysin contraction is regulated by controllers or cell tension such as RhoA, furthermore they accumulate actin and myosin at the cell cortex which generates the mechanical tension that generates the cell-in-cell invasion mechanism. The entosis mechanism can potentially have substantial energetic implication in cancer cells compared to other mechanisms of cell death and engulfment. A crucial part of the process is the active involvement of invading cells, which does not happen in other forms of cell engulfment. This allows the mechanism to selectively target living cells, excluding dead cells or non-living material such as cell debris. After internalization, engulfed cells are killed by the host cell following the maturation of the entotic vacuole that encapsulates the entotic cell. The maturation of the entotic vacuole involves modification by autophagy pathway proteins, followed by lysosome fusion and inner cell dead and degradation inside the host cell. In this mechanism, autophagy pathway proteins play an important role by scavenging extracellular nutrients derived from the inner cell death. Internalized cells can also undergo alternative fates such as apoptosis or unharmed escape from host cell. In clinical cancer specimens, evidence of DNA fragmentation has been found suggesting that non-apoptotic cell death may be a common fate for entotic cells in human cancers. Entosis correlates with cancer worse prognosis in head and neck squamous cell carcinoma, anal carcinoma, lung adenocarcinoma, pancreatic ductal carcinoma,