KRAS and neoplasm: Molecularly targeted drugs modulate the microenvironment and drive antitumor immunity.39 Selective inhibition of KRAS (G12C), which sits upstream of PI3Kα, induces a proinflammatory microenvironment with enhanced infiltration of T cells and cytokine production.40 CDK4/6 inhibitors promoted antitumor immunity by enhancing tumor antigen presentation, suppressing the Tregs, and activating CD8+T cells.41 42 These findings suggest that therapeutics originally targeting unlimited tumor cell proliferation may also act as immune modulators.