The term apoptosis was first used in 1972 to describe a morphologically distinct form of cell death. Since those early experiments and observations, apoptosis has become one of the focal points for biological research, with myriad laboratories and research groups continuing to work to further elucidate the components and pathways that drive this programmed cell death. As a fundamental biological pathway, apoptosis has benefits and adverse effects for the host organism. For example, many therapeutic strategies involve the activation of apoptosis to kill cancer cells, while other treatments seek to prevent apoptosis to preserve precious cells in key tissues. 

Once upon a time when I was a fledgling science nerd in high school, I started learning about the process of apoptosis, which remains to this day the most studied form of cell death in various functions including organismal development and defense against cancer. As an immunologist-in-training, I also learned about the classical complement pathway that the immune system uses to destroy infected cells, and also necrotic cell death or necroptosis (which is full of really gross pictures if you dare to Google it). Of course, I learned about autophagy in graduate school and really appreciate its utility in normal physiology and disease, while very recently I read about ferroptosis as yet another programmed cell death (PCD) pathway. Right around when the Nobel Prize was awarded to recognize the elucidation of PCD, pyroptosis came about as a novel PCD pathway that is continuing to gain steam in its clinical relevance. It seems logical for cells and organisms to have redundant systems in place to clear away damaged and malignant cells before a health crisis can emerge if the cell evades the primary route of apoptosis.