Discovery of immune checkpoint inhibitors has revolutionized the field of oncology. Immune checkpoints play a key role in maintaining immune homeostasis and preventing autoimmunity. Under normal situation, immune responses are regulated by a balance between co-stimulatory and inhibitory signals referred to as"immune checkpoints". Activated T cells express multiple co-inhibitory receptors such as lymphocyte-activation gene 3 (LAG-3), programmed cell death protein 1 (PD-1) and cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) that are primary mediators of immune effector responses to self-proteins, chronic infections and tumor antigens. In tumors these immune checkpoints allow the tumor cells to dodge anti-tumor response (1). Checkpoint inhibitors (CPI) block these immune checkpoints allowing the immune system to attack tumor cells (2). Although the immune system has the inherent ability to distinguish self from non-self and thus typically mount an attack on the non-self-cancer cells; over-activation of the immune response can lead to serious adverse events collectively called immune-related adverse events (irAEs) (3). While activation of the immune system and development of irAEs has been associated with better outcomes for underlying cancer (4), the associated side effects increase morbidity and mortality in addition to having a negative impact on patient’s quality of life. irAEs associated with CPI therapy can have delayed manifestation and present after the CPI have been discontinued (5).