Rooj et al. further reported physical and functional interactions between integrin-β1 and the amiloride-sensitive nonselective cation channel, composed of ASIC1, α-ENaC, and γ-ENaC, and further showed that knockdown of either integrin-β1 or α-actinin attenuated the amiloride-sensitive current [45], indicating that integrin-β1 and α-actinin may be involved in stabilizing the glioma cation channel complex and maintaining channel activity. The gene discussed is ASIC1; the disease is glioma.