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呂仁實驗室發現一種膜蛋白「Podocalyxin-like protein 1（PODXL）」對維持擴展多能幹細胞（EPSC）的增生和萬能性狀態是重要的信號傳遞機制。這對於了解早期的胚胎發育至關重要。我們發現改變PODXL在細胞中的表現量，會影響自我更新、c-MYC和端粒酶的蛋白表達量。此外，對於誘導多能幹細胞（iPSC）和EPSC的集落形成功能亦有重大的影響力。

我們是第一個團隊指出PODXL為調控膽固醇生物合成的膜蛋白，於研究中也發現人類多能幹細胞（hPSCs）對膽固醇需求比成體纖維母細胞更敏感。利用外源性膽固醇的添加完全恢復了PODXL基因減少所引起的多能性喪失。PODXL通過調節膽固醇影響RAC1/CDC42訊息傳遞來調節SREBP1和SREBP2的成熟以及脂質筏的動態。利用單細胞RNA定序顯示，PODXL過度表達和膽固醇大幅增強了在人-鼠嵌合體胚胎中人類細胞之間的嵌合性（57％）。因此，通過PODXL對膽固醇訊息傳導路徑的調控，對ESC/EPSC維持多潛能性至關重要。

利用小分子藥物將人類纖維母細胞直接重編程為視網膜前驅細胞以治療感光細胞退化。呂仁老師的團隊成功利用小分子藥物將人體的纖維母細胞轉化為視網膜前驅細胞，而非傳統的基因改造或病毒轉染方式。這一轉化過程通過動物實驗驗證了其卓越的治療效果，並且無生成腫瘤的風險。這項技術製程簡便，成本較低，而且轉化效率高，將為失明患者帶來新的希望。團隊在研究中對視網膜前驅細胞的應用發現了突破性的效果，期望為患者帶來更全面的視覺恢復治療方法。我們未來將與醫療機構和製藥公司建立合作夥伴關係，致力推動視網膜前驅細胞在細胞治療中的應用，為感光細胞退化患者帶來嶄新的治療選擇。這項重要的研究成果將成為未來光明的開端，為失明患者如夜盲症(孤兒藥)、黃斑部病變、糖尿病視網膜病變，帶來更多希望。