Just recently, KRAS G12C inhibitors have been approved by FDA.[31] Nevertheless, 85% of KRAS‐mutated cancers still lack efficient therapeutic agents.[30] The strategies to target KRAS include hindering KRAS membrane association,[32] disrupting RAS dimerization/nanoclustering,[33] interference with KRAS–SOS1 interaction,[26] inhibition of the downstream effectors,[32] synthetic lethality in KRAS mutant cancer,[34] and so on. Here, SOS1 is linked to cancer.