CCND1 and neoplasm: Other approaches of explanation include an increased DNA repair capacity due to alterations in the nucleotide excision repair (NER) system [15], an impaired mismatch repair (MMR) system with increased rates of microsatellite instability in resistant tumor samples [16–18], mutations in the BRAF V600E oncogen (26% in resistant TGCTs versus 1% in sensitive TGCTs) [17] and different mechanisms influencing apoptosis induction such as decreased activation of caspase 9 [19] or significantly higher expression of CCND1 (cyclin D1) in TGCT cell lines with artificially induced cisplatin resistance [20].