Figure 1. Receptor tyrosine kinases (RTK) recruit GRB2, SHP2 and SOS1 and load inactive KRAS (off state) with GTP to reach the active KRAS (on state). KRAS recycles through the action of Guanosine triphosphatase activating protein (GAP) back to the GDP-loaded inactive form. Mutations prevent the activity of GAPs and leave KRAS in a permanent overactive state that stimulates the downstream signaling pathways via the MAPK, PI3K and RAL cascades. The KRAS G12C can be blocked by Sotorasib or Adagrasib but no other mutated KRAS variants. The effects of mutated KRAS can be inhibited by inhibitors of the downstream signaling or cyclin-dependent kinase (CDK) inhibitors. SOS1 can be inhibited by a range of compounds including the BI-1701963, that is in clinical trials, and a range of other drugs. KRAS and SOS1 inhibitors may be combined with cytostatics to achieve more pronounced responses.