In general, the mechanisms of secondary resistance are divided between those associated with KIT/PDGFRα receptors, among which secondary mutations are believed to be most prevalent and frequent, and those mechanisms independent from KIT/PDGFRα receptors, such as (i) chromosomal alterations (such as loss of chromosomes 1p, 14q or 22q), (ii) pharmacokinetic variables, and (iii) tumor differentiation (such as sarcomatoid differentiation). Here, KIT is linked to neoplasm.