RB1 and neoplasm: The SCLC population was specifically selected to investigate the role of trilaciclib because SCLC tumors replicate independently of CDK4/6 due to inactivation of the downstream retinoblastoma (RB) protein signaling arising from high prevalence of RB loss and/or mutation; thereby, assessment of the effect on the host is feasible and devoid of potential direct effects on the tumor [11, 12].