Cancer is the leading cause of death worldwide, and its treatment and outcomes 
have been dramatically revolutionised by targeted therapies. As the most 
frequently mutated oncogene, Kirsten rat sarcoma viral oncogene homologue (KRAS) 
has attracted substantial attention. The understanding of KRAS is constantly 
being updated by numerous studies on KRAS in the initiation and progression of 
cancer diseases. However, KRAS has been deemed a challenging therapeutic target, 
even "undruggable", after drug-targeting efforts over the past four decades. 
Recently, there have been surprising advances in directly targeted drugs for 
KRAS, especially in KRAS (G12C) inhibitors, such as AMG510 (sotorasib) and 
MRTX849 (adagrasib), which have obtained encouraging results in clinical trials. 
Excitingly, AMG510 was the first drug-targeting KRAS (G12C) to be approved for 
clinical use this year. This review summarises the most recent understanding of 
fundamental aspects of KRAS, the relationship between the KRAS mutations and 
tumour immune evasion, and new progress in targeting KRAS, particularly KRAS 
(G12C). Moreover, the possible mechanisms of resistance to KRAS (G12C) 
inhibitors and possible combination therapies are summarised, with a view to 
providing the best regimen for individualised treatment with KRAS (G12C) 
inhibitors and achieving truly precise treatment.