Lung cancer, particularly non-small cell lung cancer (NSCLC), remains a major therapeutic challenge, with cisplatin resistance limiting clinical efficacy. The study under discussion identifies miR-150-3p as a tumor suppressor and cisplatin sensitizer that acts through direct downregulation of AKT2, thereby enhancing chemotherapy responsiveness. Using TCGA data and functional assays in A549 and H358 cells, the authors demonstrate antiproliferative and antimigratory effects of miR-150-3p, together with potentiation of cisplatin cytotoxicity. These findings highlight the PI3K/AKT pathway as a central mediator of drug resistance and underscore the potential of miRNA-based therapeutic strategies. Nonetheless, important limitations restrict translational applicability: reliance on only two cell lines fails to capture NSCLC heterogeneity, while tumor-microenvironment and systemic factors remain unexplored. Emerging evidence indicates that host-microbiota interactions, microbial metabolites, and iatrogenic factors such as antibiotics or proton pump inhibitors may critically modulate PI3K/AKT signaling and thereby influence cisplatin response. Moreover, challenges related to miRNA delivery and functional redundancy among AKT isoforms raise further concerns for clinical translation. Taken together, while the study provides strong evidence that miR-150-3p can sensitize NSCLC cells to cisplatin via AKT2 targeting, future research integrating in vivo models, microbiome profiling, and mechanistic dissection of AKT isoforms is required to fully assess its therapeutic potential.