Interestingly, although WT and LFS astrocytes did not differ in SOX2 expression in 2D monolayer cultured NPCs (Fig. 1a), LFS grafts exhibited significantly more SOX2 expression than WT grafts and SOX2 expression in LFS grafts was abrogated by YTHDF2 knockdown (Fig. 2d), suggesting that mutant p53 may contribute to LFS-associated tumor initiation via formation of a poorly differentiated SOX2+ cell population. The gene discussed is SOX2; the disease is neoplasm.