BY GREG BROZEIT A palpable yin-yang undercurrent shaped the course of this year’s ASH meeting. Both sides highlight the importance and value of the Myeloma Crowd Research Initiative (MCRI). On the yin side, FDA approval of daratumumab and elotuzumab and the expectation of future approvals of monoclonal antibodies are promising signs that researchers have found the trailhead of the path leading to an immunology revolution in cancer. For myeloma patients, I think there are two things to consider as this ground-breaking field of research and treatment moves forward. First, there are a number of targets in myeloma cells and there is little consensus about what just exactly each one does and how they interact with each other. Accelerated research is vital if we are to understand them completely. I hope the promise of these drugs motivates more patients to take advantage of the increasing number of immunology-related clinical trials. This will be the only way to speed up accessibility of the best drugs to the right patients. Next, the approved monoclonal antibodies as well as those currently in the research pipeline are not curative therapies. When taken, they “fix” certain mechanisms within cells, but when stopped, problems are likely to return. The ultimate goal is to create personalized immunotherapies in which a patient’s own biology and genetics can be modified to attack the harmful cause of myeloma at the cellular level. That is what both research projects of the Myeloma Crowd Research Initiative (MCRI) are striving to achieve. When the history of immunology is written decades from now, the first generation of monoclonal antibodies will be seen much like the Model T in the history of transportation. It was revolutionary but, taking the long view, the Model T was really an early step toward much greater innovations like fuel-injected and jet engines. The ideas behind MCRI are more like the jet-age than early assembly line car building. On the yang side, literally every ASH presenter mentioned—despite the unprecedented advances made in the myeloma field in recent years—the relative lack of progress achieved in myeloma high-risk disease. It was arguably the only topic of unanimous consensus at ASH. Many speakers noted that some of the new drugs “seemed to be more effective” against high-risk disease but their statements were impressions, not irrefutable conclusions. To paraphrase Ronald Reagan’s famous dictum about treaties with the Soviet Union, we need verification, not trust. Many physicians and researchers deeply believe the cure for myeloma will be found in the secrets of high-risk disease. This is why high-risk disease is fundamental to MCRI’s mission. While at ASH, I was reminded of the near giddiness cancer researchers and CML patients felt years ago when Gleevec, the first oral genetically targeted drug, was approved. When future ASH meetings are filled with that kind of exhilaration about defeating high-risk disease, we will likely have reached the Holy Grail for myeloma as well as many other cancers and immune-deficiency diseases. That’s where MCRI comes in. Unifying the yin of immunotherapy and yang of high-risk disease is integral to solving the problem of myeloma. As we embark on a New Year, I encourage you to consider making MCRI one of your resolutions. If we can successfully fund these ideas and see them through to the clinic, we can continue the marches to other key issues on the myeloma horizon.