KIT and neoplasm: This would favour the expansion of neoplastic MCs and an increasing tumour burden; in addition, it might also lead to an increased genomic instability that may facilitate acquisition and accumulation of additional genetic alterations (Table 2 and Table S1) in the KIT-mutated or unmutated HSC and contribute to the malignant transformation of the disease via distinct molecular mechanisms, e.g., activation/repression of anti-/pro-apoptotic mechanisms [79].