HRAS and colorectal cancer: Of note, much of the data presented by Rabara et al, including 1) the sensitivity of isogenic KRAS G13D SW48 cells to EGFRi relative to isogenic KRAS G12D SW48 cells and 2) the identification that NF1 expression is a critical variable that modulates sensitivity to EGFRi, are consistent with our model that reductions in WT HRAS-GTP and WT NRAS-GTP underlie the sensitivity of KRAS G13D colorectal cancer cells to EGFRi [17].