The heatmap shown in Figure 7 emphasizes that AML patients in Group A (showing high PFKM/low MAP1LC3B/low BNIP3 expression and poor prognosis) were characterized by the upregulation of a range of transcripts involved in oncogenic pathways, including glucose transporters (SLC2A1, SLC2A4), lactate/pyruvate transporters (SLC16A1), amino acids transporters (SLC6A9, SLC15A10), positive cell cycle regulation (CCNB1, CCNB2, CCNA2), and the biosynthesis of cofactors (NMNAT3, GCLM, HMBS). The gene discussed is SLC16A1; the disease is acute myeloid leukemia.