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CONCLUSIONS Our findings support a model in which cigarette smoke exposure is associated with MKK3/p38 MAPK activation and PRKN Ser131 phosphorylation, accompanied by impaired PRKN-dependent mitophagy and increased epithelial senescence markers in vitro and in vivo

Similar to TP53 mutations, KRAS mutations occurred early in carcinogenesis of the lung, and 66 percent of the mutations in the KRAS gene in smoking-associated lung tumors were GCTA transversions (Keohavong et al

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So instead of producing smoke, it produces vapour that doesn't contain the same by-products that cigarette smoke contains

Despite the benefits of the IV nicotine delivery paradigm (e.g., Our study has important implications for tobacco regulatory science