Pathological PHGDH overexpression is orchestrated by lineage-specific oncogenic drivers (e.g., EWS-FLI1 in Ewing sarcoma [5], MYC in medulloblastoma [3]), stress-responsive transcription factors (e.g., ATF4 under nutrient deprivation [9, 10]), and RNA epitranscriptomic modifications (e.g., m6A/IGF2BP3 stabilization [37]). Here, ATF4 is linked to medulloblastoma.