In breast cancer tissue, SOCS5 expression was inversely related to the tumour TNM stage [258], and, in a recent report, exogenous expression of SOCS5 (as well as SOCS1 and SOCS3) in the highly aggressive anaplastic thyroid cancer cells has been shown to reduce or abolish STAT3 and STAT6 phosphorylation and PI3 K/AKT pathway activation and resulted in alteration in the balance of proapoptotic and antiapoptotic molecules and sensitisation to chemotherapeutic drugs in vitro [262]. The gene discussed is SOCS3; the disease is neoplasm.