They originate through membrane shedding from cancer cells with an amoeboid phenotype, a process which can be induced through overexpression of oncoproteins [e.g., myristoylated Akt1, heparin-binding epidermal growth factor, and caveolin-1 (Cav-1)], silencing of the cytoskeletal regulator Diaphanous-related formin-3, or activation of Akt1 and EGFR pathways. The gene discussed is AKT1; the disease is cancer.