Open questions remain to be answered: (i) is the functional output of KRAS signaling essential for promoting tumorigenesis?; (ii) is the suppression of KRAS the dominant signalling effect in glioblastoma?; (iii) what are the general physiological effects of let-7 miRNA dysregulation in brain tumours (if any)?; (iv) are oncogenic inhibitors currently in clinical trials for KRAS-driven cancers suitable for therapeutics in KRAS wild-type tumours? Here, KRAS is linked to cancer.