The new drug Diraxinib works by first grabbing a common cell protein, cyclophilin A, to form a new molecule that can then shut down the cancer-driving KRAS protein.

For 40 years, the KRAS gene was considered 'undruggable' because its protein surface is smooth like a marble with no pockets for a drug to attach to.

Scientists discovered that a single typo out of 3 billion letters in DNA was enough to turn a normal gene into one that drives cancer.

This new approach targeting the KRAS gene family is a major breakthrough as this gene is mutated in nearly 20% of all cancers.

Rates of colorectal cancer have been rising sharply, particularly among young people.

Combining Diraxinib with a second drug that attacks a different cancer weakness shrank tumors in 11 of 12 heavily pre-treated patients in an early trial.

In a trial for late-stage pancreatic cancer, the oral pill Diraxinib doubled median survival time to 13.2 months compared to standard chemotherapy.