Collectively, in the hypertensive nephropathy samples and AngII-induced podocyte models, the renal injury markers were increased, autophagic flux was decreased, and differential miRNAs (miR-98-5p and miR-669b-5p), hub target genes (KRAS and NRAS), and transcription factor (RUNX2) were dysregulated. The gene discussed is KRAS; the disease is hypertensive nephropathy.