Sometimes, while investigating one question, scientists learn the answer to an entirely different one. Some of the most significant medical breakthroughs have begun with open-ended curiosity: insulin, for example, was discovered after two German doctors removed a dog’s pancreas in 1890 to better understand its role in digestion.

Because cancer cells proliferate at a higher rate than normal cells, they require more energy than normal cells, and thus need to rewire the cell’s energy-producing processes to meet this excessive demand. Think of spoiled Veruca Salt in Charlie and the Chocolate Factory rerouting the chocolate bar supply directly to her father’s factory, where his workers unwrapped them faster than any normal child could, expediting her discovery of a Golden Ticket.

Pancreatic cancer, which will affect an estimated 60,430 Americans this year, is notoriously hard to treat. Chemotherapy and immunotherapy drugs sometimes work at first, but often the tumors develop resistance and continue to grow. This makes it one of the most lethal types of cancer, with the average five-year survival rate after diagnosis hovering around 10%.

A range of genetic disturbances can result in the same type of cancer, the way an off-tasting dish might result from any number of bad ingredients or missteps in the preparation process. Often, variation in clinical features—tumor appearance, location, behavior—is what defines cancer subtypes, while the genetic origins of each subtype remain unclear. But to make sense of this variation, and thus refine diagnosis and develop more precise treatments, researchers must trace these clinical features back to their genetic origins.

Clear cell renal cell carcinoma (ccRCC), which accounts for over 75% of kidney cancer diagnoses, gets its name from how the tumor cells look under a microscope. Their clear appearance, as if the tissue were studded with air bubbles, is due to an accumulation of cholesterol in the cells. Studies have shown that ccRCC cells contain at least twice as much cholesterol as normal kidney cells, and in some cases up to 35 times more. How this accumulation occurs and how it contributes to cancer progression, however, is poorly understood.