LGGs are characterised by an over-activated MAPK signalling in consequence to oncogenic alteration of BRAF or FGFR1 [15] and the main hypothesis for a slow tumour evolution in LGG is based on the induction of oncogene-induced senescence which gives a growth advantage in a restricted window during brain development [7, 8, 27, 35, 40]. The gene discussed is BRAF; the disease is neoplasm.