Although recent integrative genomic analyses have implicated recurrent mutations in TP53, ATRX, PTEN, and MEN1, as well as homologous recombination deficiency (HRD), in the pathogenesis of ULMS (12–14), transcriptome-wide integrative studies—especially those aimed at uncovering shared tumorigenic mechanisms rather than subtype-specific alterations—remain limited. Here, TP53 is linked to hypoparathyroidism-retardation-dysmorphism syndrome.