Two separate preclinical advances aim to overcome solid tumor barriers for cellular immunotherapy. Columbia University researchers reported ultra‑sensitive HLA‑independent T (HIT) receptors that detect vanishingly low CD70 levels and eradicated kidney, ovarian and pancreatic tumors in models; their results appeared in Science and redefine targetable antigen expression thresholds. In parallel, investigators identified NR2F6 as an intrinsic checkpoint whose deletion markedly enhanced CAR‑T activity and tumor immunity in preclinical studies. Both approaches — receptor sensitivity tuning and removal of inhibitory nuclear receptors — address antigen paucity and T‑cell exhaustion, the principal obstacles to CAR‑T success in solid malignancies. These mechanistic leads provide two orthogonal strategies that companies and academic labs can translate into engineered cell programs or combination regimens for first‑in‑human testing.