EGFR and colorectal carcinoma: In our study, we discovered that the rebound wild-type RAS isoforms predominantly activated downstream p-ERK and p-AKT, as the co-treatment of MRTX1133 and EGFR inhibitors led to potent inhibition of ERK and AKT in both KRASG12D-mutated CRC cells and organoids (Figs. 5, 6).