N-cadherin induced anoikis resistance by recruiting PI3K.[25] Cancer cells could adapt to the loss of anchorage and generate anoikis resistance by activating EGFR family members[26] or MAPK/ERK signaling pathway-mediated suppression of BIM.[26,27] In addition, anoikis was an apoptotic process indeed, so it was also modulated by both intrinstic and extrinsic apoptotic pathways.[28] These abovementioned perspectives provided powerful support for the results of GO and KEGG pathway analysis. Here, BCL2L11 is linked to cancer.