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To do this, they created a sort of evil FOXO4 twin called a FOXO4-DRI peptide it looked and acted like FOXO4 from a chemical perspective (in fact, p53 liked to bind with FOXO4-DRI even more than regular FOXO4, which is important because of some complicated chemistry), but FOXO4-DRI didnt only live in the nucleus it could exist anywhere in the cell

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[8] This supports the involvement of ERK1/2 under the study conditions, but it does not prove that ERK1/2 is the only pathway involved or that it sits directly below FAK in a single BPC-157 signaling chainthe FAK and ERK findings came from different experimental systems

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