KIT and neoplasm: Importantly, these studies have put in evidence the polygenic character of the TGCT tumor model, identifying candidate culprit single nucleotide polymorphisms (SNPs) implicated in several distinct pathways, from the well-known KIT-KITL to DNA damage repair (namely RAD51C and BRCA1), from sex determination/germ cell specification (namely DMRT1, ZFPM1, and PRDM14) to apoptosis/cell cycle (including GSPT1 and CHEK2), from telomere maintenance (including TERT and ATFIP) to centrosome organization/microtubule assembly (TEX14, PMF1, and CENPE) [17,19,37].