Because the 1p/19q co-deletion is primarily observed in oligodendrogliomas4,5 and with additional mutations in IDH, TERT promoter, and other genes (eg, FUBP1 or CIC),12–14 we hypothesize that a proper cell type (eg, oligodendrocyte progenitor cells and oligodendrocytes), a permissive cellular microenvironment, and the presence of coordinating mutations (eg, IDH, TERT promoter, and FUBP1 or CIC) are required to confer growth advantages to cancer cells with the 1q/19p hybrid chromosome and the 1p/19q co-deletion. The gene discussed is TERT; the disease is cancer.