SOAT1 and neoplasm: The emergence of a resistant tumor during or after therapy may involve intrinsic genetic drift toward a more malignant undifferentiated phenotype with upregulation of DNA damage repair, checkpoint proteins, T cell exhaustion, and evasion of cell death through the activation of alternative signaling pathways such as Jak/STAT, NFkB, or PI3K/AKT/mTOR pathways [31,32].