SOAT1 and acute lymphoblastic leukemia: T-ALL is characterized by heterogenous genomic alterations: transcriptional activation of several protooncogenes, deletions of tumor suppressor genes, epigenetic deregulation, ribosomal dysfunction, altered RNA stability, cell-cycle dysregulation, and disordered signaling in the crucial pathways (NOTCH1/FBXW7, PI3K/Akt/mTOR, RAS/MAPK, and IL7R–JAK–STAT) [13].