This finding appears to be a unique feature of the CTLA-4 pathway, with other co-inhibitory and co-stimulatory T cell pathways, including LAG-3 and T-cell immunoglobulin domain and mucin domain 3 (TIM-3), playing a secondary role to further sculpt the magnitude and durability of the T cell response and potentially address resistance mechanisms within the tumor microenvironment [71]. Here, HAVCR2 is linked to neoplasm.