Phorbol derivatives work primarily by interacting with protein kinase C (PKC), although they can interact with other phospholipid membrane receptors.  The esters bind to PKC in a similar way to its natural ligand, diacylglycerol, and activate the kinase.  Diacylglycerol is degraded quickly by the body, allowing PKC to be reversibly activated.  When phorbol esters bind to the receptor, they are not degraded as efficiently by the body, leading to constitutively active PK.  PKC is involved in a number of important cell signaling pathways.  Thus, phorbol ester exposure can show a wide range of results.  
The main results of phorbol exposure are tumor promotion and inflammatory response.  Although phorbol is not a carcinogen itself, it greatly enhances the action of other substances and promotes tumor proliferation.  PKC is a key component in biological pathways controlling cell growth and differentiation.   When phorbol esters bind to PKC, cell proliferation pathways are activated.  This effect greatly promotes tumors when the cells are exposed to even a sub-carcinogenic amount of a substance.  
PKC is also involved in activation of inflammation pathways such as the NF-κB pathway.  Thus, exposure to phorbol products can induce an inflammatory response in tissues.  Symptoms can include edema and pain, especially to the skin and mucus membranes.
While phorbol itself does not have irritant activity, nearly all phorbol esters are highly irritant, with a wide range of half-maximal inhibitory concentration (IC) values.  The median lethal dose (LD) of phorbol esters for male mice was found to be about 27 mg/kg, with the mice showing hemorrhage and congestion of pulmonary blood vessels, as well as lesions throughout the body.