In fact, KIT expression was observed in 95% of GIST, as a diagnostic algorithm using upfront immunohistochemistry (IHC) markers of KIT (CD117) positivity in GIST [30], and with IM treatment, KIT transcript or/ and protein derived from multiple heterogeneous KIT mutations in IM-resistant cells is higher than that in pre-IM counterparts [31–33], implying the compensatory up-regulation of KIT possibly contributing to secondary resistance to IM. The gene discussed is KIT; the disease is gastrointestinal stromal tumor.