Because SOCS1 requires the SOCS box to form acomplex with ATM, v-Abl- or Pim kinase-mediated phosphorylation couldpotentially interfere with this interaction and block p53 activation.Therefore, it appears that aberrant phosphorylation by oncogenic kinases couldinterfere with the tumor suppressor activities of SOCS1 by at least twodifferent mechanisms: phosphorylated SOCS1 would not be able to inhibit theJAK/STAT pathway and to interact with ATM and promote p53 activation. The gene discussed is SOAT1; the disease is neoplasm.