Anoikis resistance appears to be critical for the aetiology of CTCs.180–182 CTCs from prostate cancer cells lose their adhesive capacity through downregulation of E-cadherin, γ-catenin and β4 integrin with, in parallel, the gain of anti-apoptotic mechanisms increasing their resistance to cytotoxic stresses induced by immune cells.183 Among them, the authors observed a decrease in heat-shock protein 90β family member 1 (HSP90B1), a chaperone protein that not only enables escape from immune surveillance, but also increases Bcl-2 under the control of Akt pathway signalling activation. The gene discussed is AKT1; the disease is prostate carcinoma.