CD40-targeting therapies aimed at augmenting the priming of tumor-specific T cells have the potential to increase response rates in approved indications where ICI therapies have limited efficacy, as well as expand the scope of eligible immunotherapy indications [1], by making the tumors more inflamed via pathways such as type I interferon [8], effectively turning immunological cold tumors hot [9]. The gene discussed is CD40; the disease is neoplasm.