Approximately 90% of mutations are mutually exclusive activating mutations in oncogenes RAS (~13%) and BRAF (~60%), and rearrangements involving RET, ALK and NTRK genes (~5%); whilst the remaining 10% are loss-of-function mutations affecting tumour suppressor genes such as PTEN, PPARγ and TP53 [17,18,19] Targeted therapies are in use for tumours with some of these mutations. Here, ALK is linked to neoplasm.