We further showed that novel TRPV4 p.M713V/I mutants lead to increased constitutive and stimulated channel activity, in addition to sustained activation of the MAPK/ERK pathway.13 Notably, we identified in additional GCLJ tumours wild-type for TRPV4 either KRAS or FGFR1 gain-of-function mutations, leading us to suggest that activated MAPK/ERK pathway promotes the genesis of sporadic and syndrome-associated giant cell rich lesions.13 14. This evidence concerns the gene TRPV4 and neoplasm.