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Seeing as disrupted lamellar bilayers (LB) may feasibly be the result of a deficiency of IGF-1 and/or a IR mutation, I hypothesize that the results of insufficient bioavailability of IGF-1 and its effects on subsequent pathway signaling likely result in the delayed processing of LB contents as seen in the KP biopsies due to the failure to regulate differentiation as skin cells mature and differentiate at the SC-SG interface