Recurrent mutations in T-ALL affect genes involved in transcriptional processes (BCL11B[19], RUNX1[20], GATA3[21]), epigenetic regulation (DNMT3A[20,22], members of polycomb repressor complex (PRC2)[21]), JAK/STAT signalling[21,23-25] (JAK1/2/3, IL7R), ribosomal processes (RPL10, RPL5)[25], and various other functions (e.g. WT1[26], CNOT3[25], PH[[27], MEF2C[28,29], LEF1[30]). This evidence concerns the gene SOAT1 and acute lymphoblastic leukemia.