STAT5A and neoplasm: Calabrese and co-workers (2009) [54] showed that the inactivation of SOCS1 disabled the p53-dependent senescence in response to oncogenic STAT5A and radiation-induced apoptosis in T cells, corroborating the results of inhibition of tumor growth and the upregulation of this gene in HL_HPS_R and indicating that SOCS1 could be a key gene in inhibiting tumor growth.