Recently, drug development has shifted to the discovery of druggable targets based on tumor biological functions of SCLC [41], theses include aurora kinase inhibitor targeting MYC amplification [42] as an enhancer of zeste homolog 2 (EZH2) inhibitor [43], poly [ADP-ribose] polymerase (PARP) inhibitors and Wee1 inhibitors targeting homologous repair machinery and DNA damage response pathway [41,42,43,44,45]. This evidence concerns the gene MYC and neoplasm.