142 Ba/F3 clones resistant to either sotorasib or adagrasib, of which 124 (87%) harbored secondary KRAS mutations. There were 12 different secondary KRAS mutations. Y96D/S was resistant to both inhibitors. A combination of novel SOS1 inhibitor, BI-3406, and trametinib showed potent activity against this resistance. While G13D, R68M and A59S/T which were highly resistant to sotorasib remained sensitive to adagrasib, Q99L was resistant to adagrasib but sensitive to sotorasib.