Thus, although the commonly used inflammation-driven cutaneous carcinogenesis mouse model (DMBA-TPA; also used in this study) exhibits recurrent mutations in genes similar to those mutated in human cSCC (Hras, Kras, Rras2 or Trp53)(Nassar et al., 2015), the low level of mutations may alter the immunogenicity and the microenvironmental niche in which the tumour grows, which may in part explain the paradoxical role of IgE in this model. This evidence concerns the gene TP53 and neoplasm.