c Myc uses different mechanisms for activating and repressing gene expression.Various microRNAs negatively determine Fbw7 expression including miR 27a, miR 182, miR 36392, and miR 223 and may raise the expression of Fbw7 regulated target genes including Notch1, Mcl 1, c Jun, c Myc, and Cyclin E. miR 451 ALK inhibitor and miR 709 suppressed oncogenesis in Notch1 induced mouse T ALL. miR 150, which can be upregulated upon thymocyte maturation, targets Notch3 and thus regulates T cell proliferation and survival. miR 326 functions in a feedback loop with Notch signaling. e p53 induced miR 34a also targets the Notch1 receptor as well as its ligand DLL1. Reduction of Notch activation in cutaneous T cell lymphoma by GSI therapy led to changes in the microRNA prole of the cell. Amongst others, miR 181a, miR 27a, miR92b, miR 18a, miR 19b, miR 222, and miR 221 were down-regulated, while miR 122 and miR 214 upregulated. miR 27a targets Fbw7/hCDC4, the substrate recognition hemopoietin element of the SCF ubiquitin ligase complex that targets Notch1 for degradation. Elizabeth repressive influence of miR 27a on mRNA is very pronounced at the early G1 stages and G2/M. us, GSI might ultimately deregulate Notch1 through the miR 27a Fbw7 pathway. Other objectives of miR 27a includes BTB10, which serves as a repressor of Sp transcription factors and causes G1 charge, and the transition is inhibited by the Myt 1 kinase, which through G2 M by improved phosphorylation and inactivation of Cdc2. miR 27a is frequently upregulated in pediatric B ALL. Up-regulation of miR 122 by GSI seems to be mediated by p53 and comes with an antagonistic effect on apoptosis through activation of Akt. H Myc is, among others, a target of Notch natural product libraries and has broad effects on tumorigenesis and modulates GC induced apoptosis. Conditional over-expression of c Myc in hematopoietic cells in mice culminated in the synthesis of malignant T cell lymphomas and acute myeloid leukemias. c Myc can also be activated in T ALL independently of Notch1. ese authors demonstrated a role for the PI3K/Akt axis in c Myc service. Dysregulation of the c Myc gene is just a common characteristic of Burkitts lymphoma because of chromosomal translocations, the most frequent one being t concerning c Myc and IgH. Other hematopoietic malignancies known with c Myc overexpression contain diffuse large B cell lymphoma, follicular lymphoma, CLL, B cell lymphoma, and AML. Earlier studies have shown that dexamethasoneinduced apoptosis of a T ALL cell line was related to d Myc reduction. e GC mediated down-regulation of c Myc phrase was regarded as one mechanism that plays a part in apoptosis. Not all reports have conrmed this nding, which might be explained by the many signaling pathways induced by GCs.