It became obvious that Peter Vandenabeele was a troublemaker when, after establishing himself as one of the early researchers on cell death, he challenged the dichotomy argued by others that programmed or regulated cell death consisted of autophagy and apoptosis. While others argued that cell deaths were either uncontrolled necrosis or variants of autophagy or apoptosis, he argued that other types of death were sufficiently consistent in pattern and characterized by distinct enzymatic pathways to merit their own categorization and name. Among the patterns that he and his group identified were necroptosis, previously categorized as necrosis but for which he identified distinct roles for kinases and a constrained leakage from cell membranes, releasing Damage-Associated Molecular Patterns that induced responses by the immune system and thereby led to a more aggressive response by the immune system, an important element in defeating cancer. His pursuit of this topic led him to accept and emphasize yet another form of cell death, ferroptosis, an iron-requiring form of cell death that is characterized by the accumulation of lipid droplets in cells. At meetings and conferences, he can always be counted on to ask stimulating, challenging, and provocative questions. He directs a large group at one of Europe’s largest and best-known cell death centers. Given his broad interests, he has developed a large library to screen for the responses of tumors to many drugs and to silencing of kinases, ubiquitylating enzymes, and other enzymes with short hairpin and short interfering RNAs. Thus, his group has become a leader in the search for molecules that can suppress cancers through modulation of apoptosis, phagocytosis, necrosis, ferroptosis, and immune responsiveness. We look forward to many years of contributions from this laboratory regarding the numerous general and specific biochemical mechanisms of cancer and many other diseases, the vulnerable pathways that they manifest, and how to treat them.