While the contribution of ion channels toward medulloblastoma tumorigenesis and progression are very poorly explored, a recent study reported EAG2, that shares similar electrophysiological properties with EAG1, to be overexpressed in a significant subset of mouse and human medulloblastoma across molecular (WNT, SHH, or Group 4) and histological (nodular, classic, desmoplastic, or anaplastic) subgroups and to control mitotic entry and tumor growth 36. The gene discussed is SHH; the disease is medulloblastoma.