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The mechanism isn't absorption rate (subcutaneous bioavailability remains consistent regardless of time)

Such disruption includes mutations in methyl-CpG-binding protein 2 ( MeCP2 ), 104,105 activity-dependent neuroprotective protein ( ADNP ), 106 engrailed 2 ( EN2 ), 107 voltage-dependent calcium channel subunit 1C ( CACNA1C ), 108 T-box brain 1 ( TBR1 ), 109,110 myocyte enhancer factor 2C ( MEF2C ) 111 and de novo deletions or duplications in 15q11-q13 (which cover ubiquitin-protein ligase E3A ( UBE3A ))

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Furthermore, oxidative stress activates the release of HMGB1 signal transduction in keratinocytes by decreasing the level of melanogenetic molecules (including gp100) and inducing apoptosis