Targeted approaches, including BH3 mimetics (e.g., venetoclax) for BCL-2-dependent T-ALL subtypes [107,108,109], mTOR inhibitors (e.g., everolimus) for PI3K/Akt/mTOR pathway activation [102,103], and JAK/STAT inhibitors for IL7R/JAK/STAT-mutated T-ALL [97,98,99,100], are expanding the therapeutic landscape and may be integrated with conventional regimens to optimize efficacy while minimizing toxicity [104,111,112,113]. This evidence concerns the gene SOAT1 and acute lymphoblastic leukemia.