All these data indicate that BK channels do not contribute to the basal 2D migration, consistent with the finding that at the resting [Ca2+]i (100–200 nM; Bordey et al., 2000; Kraft et al., 2003) and membrane potential of GBM cells (−50 to −20 mV; Ransom et al., 2002; Fioretti et al., 2009), the BK channel activity is close to zero (see Ramson et al., 2002 for GBM BK channel activity at varying [Ca2+]i and membrane potentials). The gene discussed is KCNMA1; the disease is glioblastoma.