In regard to the expression and role of TRPML channels in gliomas, we previously reported that TRPML2 silencing inhibits cell viability and proliferation [22] and increases the invasion [23] in T98 and U251 GBM cells; activation of TRPML1 channels by the MK6-83 agonist inhibits cell viability and induces apoptosis in T98 and U251 cells [24] and silencing of TRPML1 promotes the survival and invasion capability in T98 and U251 cells by affecting the autophagy and cell senescence processes [25]. Here, MCOLN2 is linked to glioblastoma.