Recent studies highlight the functional heterogeneity of PAX7 across cancer types: in solid tumors like rhabdomyosarcoma and glioblastoma, PAX7 overexpression drives oncogenic transformation and metastasis, whereas in hematological malignancies such as acute myeloid leukemia, its role remains context‐dependent, potentially suppressing differentiation or promoting survival depending on genetic codrivers [12, 13]. Here, PAX7 is linked to glioblastoma.