In this context, wild-type (full length) ALK is susceptible to single-base pair missense mutations in key regulatory regions of the tyrosine kinase domain, thereby perpetuating ligand-independent signalling through disrupting the auto-inhibited allostery of the active-site [151]—namely three key ‘hot spot’ mutations which account for 85% of ALK mutations in neuroblastoma; R1275, F1174, and F1245 [152]. Here, ALK is linked to neuroblastoma.