KRAS and neoplasm: Further on, the identification of BI-3406 in pre-clinical studies (a highly potent selective small-molecule SOS1 inhibitor that binds to the catalytic domain of SOS1 thereby prevents the interaction with KRAS) allowed for broadening the spectrum of activity by demonstrating that the therapeutic efficacy of this molecule was not limited only to KRAS c.34G > T (p.G12C) mutant models but also showed activity in KRAS c.35G > T (p.G12V) (SW620cells), KRAS c.38G > A (p.G13D) (LoVo cells) and KRAS c.34G > A (p.G12S) (A549 cells) as well by inducing tumor growth inhibition in xenograph models [213].