Furthermore, by using ARS-853 as a molecular tool, a study found that KRAS (G12C) is rapidly cycling rather than in a statically active state, that KRAS (G12C)-mediated signalling can be regulated by upstream effectors, and that cell viability and growth depend on KRAS mutations to varying degrees even within KRASG12 cancer cell lines120,123. This evidence concerns the gene KRAS and cancer.