The resistance to apoptosis is a fundamental feature of malignant cells, and several mechanisms are described to induce apoptosis resistance in CTCL, such as the activation of the NF-κB pathway [36], delayed expression of FasL following activation [37], diminished FAS/CD95 expressions [38], downregulation of the TRAIL pathway [39] and loss of TNFR1 with a high level of IER3 expression, among other factors [38]. This evidence concerns the gene NFKB1 and primary cutaneous T-cell non-Hodgkin lymphoma.