The activities against fibrosarcoma and neuroblastoma rat cells and human T-leukemia cells can be described by a mechanism that induces the formation of transmembrane pores allowing the peptide to enter the cytoplasmic compartment of the cancer cell, co-localize with negatively-charged mitochondria and consequently depolarize them, resulting in cytochrome C release or activation of the caspase cascade, thereby leading to cell death via apoptosis (Figure 1) (Mader et al., 2005; Pepe et al., 2013). The gene discussed is CYCS; the disease is cancer.