Based on the proposed models of protein sorting to intra-luminal vesicles of the MVBs, exosomes internalized into cells via clathrinmediated endocytosis are postulated to enter the endosomes for sorting, and are either sent to the lysosomes for degradation or repackaged into the host’s exosomes in an ESCRT-dependent manner. Alternatively, exosomes may directly fuse with cellular membranes and unload their cargo proteins into the target’s cytosol. Thus, the non-specific uptake of cytosolic proteins during inward budding processes and/or transient association between cytosolic proteins and transmembrane proteins may possibly lead to sequestration of the newly acquired proteins into the re-packaged exosomes. Translation of exosomal mRNA can also play a role in the target cell’s exosomal protein composition. Exosomes may encapsulate transferable and functionally active mRNA, and exosomal mRNA newly transferred into the target cell’s cytosol may be translated by free-floating ribosomes. Thus, newly translated cytosolic proteins may be sequestered into the target cell’s ILVs of the MVBs during inward budding processes, and consequently packaged and released in exosomes. In addition to proteomic changes, microarray analysis revealed that the interplay between 231-derived exosome-like microvesicles and HSG cells altered the mRNA composition of HSG-derived exosome-like microvesicles. The literature suggests that interactions between exosomal ligands and cellular receptors can induce cellular activation,Genistin leading to nascent mRNA transcripts. Therefore, the direct fusion of exosomes with the target cell can lead to unloading of exosomal mRNA into the cytosol where basal inward budding processes occur and trigger the sequestration of novel exosomal mRNA into newly synthesized exosomes. Here, we showed that the interplay between 231-derived exosome-like microvesicles alters HSG-derived exosome-like microvesicles both transcriptomically and proteomically. However, because this is an in vitro study, we are unable to make the assumption that breast cancer cell-derived exosomes induce breast cancer-specificbiomarkers released from the salivaryglands. Instead, based on our observations, we can suggest that within an in vivo setting, if breast cancer-derived exosome-like microvesicles were to reach the salivary glands, and if breast cancer-derived exosome-like microvesicles are internalized by the salivary gland cells, the composition of released salivary gland-derived exosome-like microvesicles will change both transcriptomically and proteomically. The mechanism underlying the alteration of HSG-derived exosomal composition is unknown. However, previous findings in Glycitein regards to exosomal biogenesis and cellular cargo trafficking provide us a solid foundation for further investigation. Examining how acquired cancer-derived exosomal contents are packaged in salivary gland cell-derived exosomes will be crucial for decoding the mechanism underlying the existence of salivary biomarkers. Furthermore, understanding how cancer-derived exosomes enter the salivary gland cells will provide us with a clue as to whether salivary biomarkers are directly derived from the disease source or whether secondary messengers are involved. MPH has been shown to have addictive potential, although it is not abused as frequently as cocaine. Recent studies have detailed an increasing incidence of MPH abuse among young adults and college students in the United States, most likely for its purported non-therapeutic benefit of cognitive enhancement also called ‘‘neuroenhancement’’.