It is well‐established that gain‐of‐function mutations of PIK3CA play critical roles for aberrant AKT activation in various human cancers.[18, 19] Consistent with these reports, patient‐derived oncogenic mutant PIK3CA‐H1047R[20] could markedly activate AKT in Ctr1‐proficient, but not in Ctr1‐deficient MEFs or CTR1‐depleted tumor cells (Figure 2a,b). The gene discussed is SLC31A1; the disease is cancer.