HMGB1 and neoplasm: Bald et al. showed that UV irradiation not only triggers tumor-initiating DNA alterations in melanocytes, but also stimulates their metastatic spread through TLR4 (toll-like receptor 4)/MyD88 (myeloid differentiation primary response 88)-driven neutrophilic inflammation originating from HMGB1 (high mobility group box 1) release from UV-damaged keratinocytes [87].