KRAS is the most commonly mutated oncogene in human cancer, and for decades its smooth, pocket-free surface made it "undruggable." This simulator renders a live population of KRAS molecules as a rotatable 2D-projected cloud, each one independently cycling between an inactive GDP-bound state and a signalling-active GTP-bound state under a real stochastic two-state switch. Dialling in a sotorasib-like covalent inhibitor exploits a cryptic pocket that only the G12C mutant exposes while GDP-bound, irreversibly locking molecules off one at a time — while the wild-type control stays completely unaffected, and an optional resistance mutation shows exactly how tumours escape the drug in the clinic. A live line chart and a state-transition network panel track the active GTP fraction, the drug-locked fraction, downstream ERK signal, and the resulting net tumour growth rate as the population responds in real time.