At the molecular level, 5-AZA increased the expression of SOCS3, known to be among the numerous targets of STAT3 and known to be able to negatively regulate its activation, suggesting that methylation of the SOCS3 promoter could contribute to STAT3 activation in PEL cells, as previously reported in bladder cancer cells in which hypermethylation of SOCS3 represents a prognostic biomarker [40]. This evidence concerns the gene STAT3 and urinary bladder cancer.