The so-called gain-of-function somatic mutations that lead to constitutive activation of c-kit are observed in several malignant diseases, such as gastrointestinal stromal tumors [81], mastocytosis [82], acute myeloid leukemia [83], and testicular seminoma [84], whereas in the cases of small cell lung cancer [85], neuroblastoma [86], colorectal cancer [87], and ovarian cancers [88], mutations in c-kit have not been identified, but paracrine and/or autocrine activation of c-kit does occur during transformation and progression. This evidence concerns the gene KIT and testicular seminoma.