Concurrent somatic mutations and copy number alterations are frequently observed in T-ALL leading to dysregulation of several cellular pathways, including JAK-STAT signaling (IL7R, JAK1, JAK3, DNM2), Ras signaling (NRAS, KRAS, and NF1), PI3K-AKT signaling (PTEN, AKT1, PIK3CA PIK3CD), epigenetic regulation (PHF6, SUZ12, EZH2, KDM6A), transcription factors and regulators (ETV6, GATA3, RUNX1, LEF1, WT1, BCL11B), and translation regulators (CNOT3, RPL5, RPL10) [135,136,140,141]. The gene discussed is SOAT1; the disease is acute lymphoblastic leukemia.