In particular, we found that 96% of sorafenib targets, including amplifications in CCND1, BRAF, PDGFR, VEGFR, and FLT3, were subclonal events, which may explain the low efficacy of sorafenib in ICC (Figure S2B, Supporting Information).[4] We observed significant correlation between mutation‐ITH and tumor size (Pearson r squared = 0.83, P = 0.00079) as well as CNA‐ITH and tumor size (Pearson r squared = 0.67, P = 0.016) (Figure S2C, Supporting Information). The gene discussed is FLT3; the disease is neoplasm.