So in this particular case, I've listed a single interaction that exists in each one of these pathways. So in the case of Epinephrine, we said that the activated G alpha protein must go on and bind to adenylate cyclists to actually transform those ATP molecules into cyclic Amp molecules, which then go on and activate protein kinasea. So in epinephrine signaling, the ALPHAG protein must interact with adenos cyclists for that pathway to actually continue. In the case of the phosphoric cascade, we saw that the IP three has to bind onto a specific ligand gated calcium on channel on the Er membrane to actually allow the movement of the calcium from the Er lumen and into the cytoplasm. And only then can protein kinase C and the calmodulatenant protein kinase actually be activated. Now, in the case of insulin signaling, we said that the IRS one must bind onto that insulin receptor to actually act as an adaptive protein to allow the attachment of the phosphor nosetie three kinase, that specific type of lipid kinase that is needed to actually transform the pip two into the pip three molecule that we mentioned right over here.