Notably, the activation of STAT3 and STAT5 was observed in both early and late stages of CTCL, and upregulation of STAT5 at the beginning of the disease is correlated with increased expression of micro-RNA miR-155, that targets STAT4, which is important for proper T-helper 1 (Th1) differentiation, and this disruption is considered to be one of the molecular mechanism contributing to CTCL development (Netchiporouk et al., 2014). This evidence concerns the gene STAT4 and primary cutaneous T-cell non-Hodgkin lymphoma.