In breast cancer, CFTR has been shown to promote cell proliferation and migration by activating the PI3K/Akt signaling pathway.[71] In colon cancer, CFTR expression is associated with increased invasiveness and metastasis.[72] Similarly, in lung cancer, CFTR overexpression is correlated with poor patient prognosis and increased tumor growth.[73] Another channel that has been implicated in cancer is the chloride intracellular channel 1 (CLIC1).[74] CLIC1 is a member of the glutathione S‐transferase (GST) superfamily and is known to regulate cell proliferation and survival. The gene discussed is AKT1; the disease is breast cancer.