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Following UV radiation, many inflammatory mediators (such as inflammation-associated cytokines, chemokines, prostanoid-synthesizing enzyme COX-2 and lipid mediators) are released from cells residing in the skin, which is likely to be mediated by the UV-induced release of self-RNAs as a damage-associated molecular pattern dependent on Toll-like receptor 3 (TLR3) and Toll-like receptor adaptor molecule 1 (TRIF) from keratinocytes [104, 125, 126]

And the turnover of cells in the gut is in many ways the same sort of turnover process that's involved in wound healing and repair

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The risk exists only for opioid-receptor-active peptides (certain enkephalin analogs) that are explicitly scheduled