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On the other hand, albumin can also decrease endogenous cellular PP-IX accumulation and protein aggregation by acting as a “PP-IX sponge.” Thus, albumin may shift the equilibrium of PP-IX homeostasis and possibly act as a novel genetic modifier of porphyric tissue damage by mediating speciation.[93] Loss or gain-of-function mutations in cellular transporters of porphyrin may serve as genetic modifiers by sequestering porphyrins or expanding their uptake, consequently intensifying disease symptoms