Notably, this dependency on MCL-1 has also been demonstrated in oncology, where single-cell RNA-sequencing revealed that therapy-induced senescent tumor cells expressed high MCL-1 levels across both BCL-2+ and BCL-2− clusters, suggesting that MCL-1 functions as an alternative or complementary pro-survival pathway in senescent cells regardless of BCL-2 status. Here, BCL2 is linked to neoplasm.