Fecal Microbiota Transplantation for Ulcerative Colitis: Not Just Yet.

exome sequencing studies of sporadic tumors, this discovery is noteworthy in that it provides a new and rational target for investigation. IPMK is an inositol phosphate kinase, and the authors describe a link between IPMK and p53-mediated apoptosis. It will be important to understand the importance of this interaction in the context of homeostasis and transformation of enteroendocrine cells. Previous reports that hemizygous deletion of Ipmk in mice did not seem to result in carcinoid tumors suggest that the role of IPMK is likely to be complex. Further studies are warranted, because additional insights may be gained into other molecular partners of IPMK or critical pathways that intersect with IPMK in carcinoids. A sobering but increasingly pervasive message is that genetics may not hold the key to deciphering carcinoid tumors. A role for genetics is certainly not excluded, but alternative mechanisms must be considered. For example, the identification of multiple genes that regulate histones and chromatin in pancreatic neuroendocrine tumors and pulmonary carcinoids raises the intriguing possibility that epigenetic mechanisms may be more relevant. In addition, there may be mutations in noncoding regulatory regions of the genome that are not sequenced routinely. New hypotheses that explore whether carcinoid tumors may instead be driven by alterations in the metabolome or the microenvironment also deserve consideration. The need for discovery is great, because therapeutic options in carcinoid remain limited and inadequate. A focus on innovative “postgenetic” strategies may provide new clues to unravel the mysteries of these unconventional tumors.