One noteworthy observation is that while p38α active site labeling is unaltered, a labeling site indicative of the p38-MAPKAPK2/3 interaction generates 6.9-fold more signal in the tumor samples relative to control.[14] While some of the altered targets have been implicated in tumorigenesis, their specific impact on tumorigenesis within the colon will likely be the subject of continued research. This evidence concerns the gene MAPKAPK2 and neoplasm.